40 spine questions answered with real clinical data

Cauda equina syndrome is the only true neurosurgical emergency in spinal pathology. Its warning signs: loss of bladder or bowel control, numbness in the perianal area («saddle anaesthesia»), bilateral leg weakness. Current consensus calls for decompressive surgery within the first 24 hours. The evidence shows that surgery before 24 hours produces significantly better recovery of bladder function than delayed surgery. There is no safe window for waiting.

Other symptoms that require urgent assessment — not an emergency, but not something to postpone for weeks — are: progressive weakness in a leg or arm, a new neurological deficit, or severe night pain with no position of relief (a red flag for systemic pathology).

This is the question the diagnostic chain most often gets wrong. The SPORT trial (Weinstein et al., NEJM 2006) — the largest randomised trial on spine surgery — showed that a significant proportion of patients with a «large» disc herniation and «severe» stenosis improve without surgery over the course of months. More importantly: multiple studies document that up to 60% of asymptomatic people have «abnormal» MRI findings by age 40.

A surgical indication requires clinical-radiological correlation: the patient's symptoms must correspond anatomically to what the imaging shows. An L4-L5 herniation on a scan does not explain arm pain. L3-L4 stenosis does not explain L5 numbness on the opposite side. Imaging identifies anatomy. The clinical picture identifies the problem.

Pain is a neurological experience, not an image. There are conditions that produce intense pain with a structurally normal MRI: discogenic pain without a visible herniation (an annular fissure does not show on a standard MRI), facet joint pain (mild arthrosis produces no signal), central sensitisation (the nervous system amplifies normal signals). In chronic pain, psychological factors — catastrophising, kinesiophobia, depression — predict pain levels better than any imaging finding.

The honest answer: a normal MRI does not mean there is no real pathology. But it also means structural surgery is unlikely to resolve that pain. The diagnosis must find the real cause before any intervention is proposed.

The surgical indication is solid when three criteria are met simultaneously: (1) a clear diagnosis with verified imaging-symptom correlation, (2) documented failure of appropriate conservative treatment over an adequate period (typically 6–12 weeks for a herniation, 3–6 months for stenosis without deficit), and (3) no major medical or psychosocial contraindications.

The clearest indications — where waiting does cause harm — are: progressive neurological deficit (weakness increasing week by week), cauda equina syndrome, and cervical myelopathy with clinical deterioration. In every other case, surgery is an option — never an obligation — and timing is part of the technique.

Whenever: a spinal fusion is proposed to you, you are told there is «nothing to be done», the surgical proposal is extensive for a symptom you have had only a short time, or you are facing a reoperation. Revision surgery is the area where a second opinion has the greatest clinical impact — because diagnosing why the previous surgery failed requires specific experience that not every surgeon has.

A properly conducted second opinion does not delay treatment — it clarifies it. And in spinal pathology, where some decisions (fusion, the level operated on) are difficult or impossible to reverse, clarifying before acting is worth the time.

Inter-observer variability in spine radiology is documented and significant. Terms such as «protrusion» vs «extrusion», «moderate» vs «severe» stenosis, and «mild» vs «significant» compression do not have consistent universal definitions in the literature. A classic study showed that the same MRI was interpreted differently by different radiologists in up to 40% of cases for clinically relevant decisions.

The spine neurosurgeon who is going to operate on you must read the original images, not the report. The report describes what the radiologist saw. The surgeon determines whether that explains your symptoms. These are two different questions. Always bring the disc with the images, not just the printed report.

They are both, depending on context. The study by Boden et al. (J Bone Joint Surg, 1990) showed that 20% of asymptomatic people under 60 and 36% over 60 have disc herniation findings on MRI. Jensen et al. (NEJM 1994): 52% of people with no symptoms at all have a disc protrusion. Disc degeneration is part of ageing, not a disease in itself.

The most frequent error is treating the image instead of the patient. «You have degeneration at L4-L5» is not a diagnosis of the cause of pain. It is a description of the anatomy of a person of a certain age. The diagnosis comes from correlating that anatomy with the specific symptoms that particular patient has.

They are degrees of migration of disc material beyond its normal boundaries. Protrusion: the nucleus pulposus bulges the annulus fibrosus without rupturing it. Extrusion: disc material crosses the annulus fibrosus but remains continuous with the disc. Sequestration: a disc fragment sits free in the spinal canal, no longer continuous with its disc of origin.

The clinically relevant paradox: sequestrations and extrusions are more likely to resorb spontaneously than protrusions. The free fragment comes into contact with immune cells in the spinal canal that actively phagocytose it. This is one of the reasons watchful waiting is frequently the correct strategy in large herniations without severe neurological deficit.

Modic changes are MRI signal alterations in the vertebral endplates adjacent to the disc. Type 1 (hypointense on T1, hyperintense on T2): active inflammatory oedema — associated with intense axial pain of discogenic origin. Type 2 (hyperintense on both T1 and T2): fatty replacement, a more chronic phase. Type 3 (hypointense on both): bony sclerosis.

Their clinical relevance: Modic 1 is one of the best predictors that axial pain has a genuinely discogenic origin (rather than muscular or facet-related). If a patient has Modic 1 at L5-S1 and pure axial low back pain that has not responded to conservative treatment, that finding points to the disc as the pain generator — information that changes management.

Yes, almost always. The surgical indication must be based on recent imaging. An MRI older than 6–12 months may not reflect the current situation: a herniation may have partially resorbed (changing the indication), stenosis may have progressed, and sagittal alignment may have shifted.

In revision surgery this point is even more critical: contrast-enhanced MRI (gadolinium) distinguishes epidural fibrosis (which enhances homogeneously and immediately) from recurrent herniation (avascular, does not enhance). Without a gadolinium MRI in a previously operated patient, the cause of failure is speculation, not a diagnosis. At CICOVE we request up-to-date imaging in every case, and with gadolinium in every patient who has had previous surgery.

Yes, and more often than most patients believe. The rate of spontaneous resorption documented in the literature is 60–70% at 12 months for symptomatic herniations. The best documented paradox in all disc pathology: the largest fragments — extrusions and sequestrations — are more likely to resorb than small protrusions. The mechanism is immunological: the free fragment in the spinal canal is recognised as «foreign material» and actively phagocytosed by macrophages.

This evidence supports a strategy of watchful waiting in patients without severe neurological deficit. The SPORT trial (NEJM 2006) confirmed that four-year outcomes of surgery versus conservative treatment in lumbar disc herniation are comparable in patients who tolerate the waiting period. What surgery does offer: faster relief of radicular pain.

There are three situations where waiting is not an option: (1) Progressive motor deficit — weakness that worsens week by week (foot drop, quadriceps weakness) justifies urgent surgery to prevent irreversible axonal damage. (2) Cauda equina syndrome — covered above: surgery within 24–48 hours. (3) Absolutely disabling radicular pain that does not respond to any conservative treatment — here quality of life takes precedence.

The key point in non-urgent cases: that the conservative treatment actually be the right one. «Rest, NSAIDs and repeated epidural injections» without active physical therapy is not appropriate conservative treatment — it is waiting without treatment. When appropriate conservative care fails at 6–12 weeks, surgery has a clear indication.

A microdiscectomy is the removal of the herniated fragment under magnification with a surgical microscope, through a 1–2 cm incision, with minimal muscle dissection. Effectiveness for radicular pain (sciatica): 85–95% in the short term. Leg pain typically improves within days to weeks; residual back (axial) pain can take longer.

What a microdiscectomy does not do: it does not «cure» the disc. The same segment can reherniate in 5–10% of cases. It does not stop the underlying degenerative process. That is why ten-year outcomes between surgery and conservative treatment in lumbar disc herniation tend to converge — surgery wins the race on symptom relief, not necessarily the one on preventing future degeneration.

Yes. The documented reherniation rate is 5–10% in the first 2–5 years. The most important modifiable risk factors are smoking and excess weight; non-modifiable ones include the anatomy of the annulus fibrosus and the level operated on. A reherniation is not synonymous with surgical failure — it is the natural history of the disc in a patient with risk factors.

Nor does reherniation mean automatic reoperation. Many reherniations can be managed conservatively again, particularly if the fragment is small and the neurological deficit is not progressive. When reoperation is required, the results of a second discectomy are comparable to the first — but each additional operation increases the risk of epidural fibrosis and complicates any eventual third surgery.

No. The crucial difference: a cervical herniation can compress the spinal cord as well as the nerve roots. Cord compression (myelopathy) is qualitatively more serious than root compression — it produces symptoms in the arms AND legs, imbalance, and can progress to quadriplegia if not decompressed. In the presence of myelopathy, watchful waiting is not appropriate.

The surgical options also differ: in the cervical spine there is anterior fusion (ACDF, the standard since the 1950s with excellent long-term results) and disc arthroplasty (ADR), which preserves motion at the segment. ADR has Level I evidence from randomised trials showing results similar to or better than fusion at 5–10 years in selected patients, with a lower rate of adjacent segment disease.

The SPORT trial for lumbar stenosis (NEJM 2008) is the strongest reference: decompression surgery produces greater improvement in pain and function than conservative treatment at four years in patients with symptomatic stenosis. The practical clinical indication: neurogenic claudication that significantly limits walking capacity (less than two blocks), without response to 3–6 months of appropriate conservative treatment.

What the trial also showed: patients who did improve with conservative treatment maintained that improvement. Not every patient with stenosis on imaging and symptoms needs surgery — only those who do not improve with time and correct treatment. Urgency increases if there is a progressive neurological deficit.

No, and this is one of the most debated decisions in spine surgery. The SLIP trial (NEJM 2016) randomised patients with L4-L5 degenerative spondylolisthesis to decompression plus fusion versus decompression alone. Result: fusion produced significantly better pain relief and function at two and four years. However, the NORDSTEN-DS trial (NEJM 2021) showed similar results between the two groups at longer follow-up.

The practical decision: in spondylolisthesis with demonstrated dynamic instability (more than 4 mm of translation on flexion-extension) or significant sagittal deformity, fusion is indicated. In stable Grade I without instability, decompression alone may be sufficient. Every case requires individual analysis — there is no universal answer.

When a spinal segment is fused, the adjacent levels compensate with greater mobility and load. Over time, this overload accelerates degeneration at those levels — this is adjacent segment disease (ASD). The documented incidence is 2–3% cumulative per year; at ten years, up to 25% of patients with lumbar fusion have symptomatic ASD requiring reintervention.

Prevention rests on: fusing the minimum number of levels necessary, respecting sagittal mechanics (not fusing in kyphosis), and considering motion-preserving techniques (arthroplasty) when the biology of the segment allows it. In revision surgery, ASD is frequently the reason for the new operation — which is why at CICOVE the planning of any fusion includes analysis of the adjacent segments and their risk of accelerated degeneration.

Partially — and the «partially» depends critically on the timing of surgery. Cervical decompression halts the progression of myelopathy in more than 90% of cases. But recovery of an already established deficit is variable: mild to moderate symptoms of less than twelve months' duration have the best chance of partial to complete improvement; severe long-standing deficit rarely recovers fully.

The fundamental principle: in myelopathy, conservative treatment has no evidence of efficacy in halting progression. Physical therapy and anti-inflammatories manage symptoms but do not decompress the cord. A chronically compressed spinal cord develops irreversible ischaemic changes. Surgery is not an option — it is the only intervention that modifies the natural history.

The following symptoms in a patient with known or unknown spinal pathology are a medical emergency — do not wait for a scheduled appointment: loss of bladder or bowel control (incontinence or retention), sudden numbness in the perianal or genital area (saddle anaesthesia), sudden bilateral leg weakness or inability to walk, rapidly progressive weakness in an arm or hand in cervical pathology.

Also: high fever with severe back pain (suggesting discitis or an epidural abscess — an infectious emergency), a history of cancer with new severe night pain (metastasis), or spinal trauma with any neurological symptom. In cauda equina syndrome, every hour of delay compromises recovery of bladder function. This is not a situation to leave until the next morning.

This distinction is the most important one a patient with spinal pathology can understand. A disc compressing a nerve root does not move because the patient takes an anti-inflammatory. A stenotic canal does not widen with physical therapy. A vertebra that has slipped does not return to position with exercises.

What conservative treatment does do — and does well when correctly applied: it reduces perilesional inflammation, improves pain tolerance, optimises neuromuscular function, and in many cases allows natural history (resorption of a herniation, adaptation to narrowing) to resolve the problem without surgery. The error is asking conservative treatment to do what it cannot: repair a structural compression that is producing a progressive neurological deficit.

Yes, but with a precise time limitation that patients should know about. Epidural injections produce significant reduction in radicular pain in the first 4–6 weeks — enough to break the pain-spasm-inactivity cycle and allow active physical therapy. However, multiple randomised trials show that at 3–6 months the effect is comparable to placebo.

In practice: they are a bridge, not a destination. In the right context (severe acute radicular pain, a herniation with active perilesional inflammation) they are a useful tool. When used repeatedly as a substitute for definitive treatment — whether appropriate conservative care or surgery — they only delay the decision. The FDA warning (2014) on intrathecal administration of particulate steroids is also relevant: technique and steroid type matter.

Yes — and more than most surgeons publicly acknowledge. The psychosocial predictors of surgical outcome with Level I evidence are: pain catastrophising (believing the pain is devastating and uncontrollable), kinesiophobia (fear of movement), active major depression, and active workers' compensation or litigation.

The study by Celestin et al. (Pain 2009) documented that patients with high preoperative catastrophising have a probability of poor surgical outcome comparable to that of patients with inadequate nerve decompression. This does not mean the pain is psychological — it means surgery resolves the structural problem but not the pain amplification system. At CICOVE we assess these factors before any major surgery, especially in revision cases.

No. The evidence against prolonged rest in low back pain is robust and consistent. The trial by Malmivaara et al. (NEJM 1995) compared bed rest, extension exercises, and continuing normal activity in acute low back pain. Result: the group that continued normal activity recovered better on every indicator than the bed rest group.

The maximum rest currently recommended in acute low back pain is 1–2 days — only for the most intense peak of pain. Beyond 48 hours, rest delays recovery, weakens the stabilising musculature, and increases the risk of chronicity. Prescribing «absolute rest» for an uncomplicated episode of low back pain has been outside the clinical guidelines of every major spine society for decades.

It depends on the case. Spinal manipulation has evidence similar to therapeutic exercise for uncomplicated acute low back pain. But it has absolute contraindications that are not always respected: active neurological deficit, disc herniation with severe root compression, cervical myelopathy, spinal instability, fracture, severe osteoporosis, anticoagulation.

The most serious documented risk is vertebral artery dissection following high-velocity cervical manipulation, which can cause a stroke. The incidence is low (estimated at 1 in every 400,000 to 2 million manipulations), but the outcome can be devastating. In spinal pathology with active neurological compression, spinal manipulation is not the appropriate tool — regardless of the practitioner's experience.

Smoking has a quantified impact in spine surgery that goes far beyond general anaesthetic risk. It doubles the rate of pseudarthrosis (non-united fusion) in spinal fusions. It increases the risk of wound infection up to threefold. It delays disc healing. It inhibits vascularisation of the bone graft.

Nicotine produces vasoconstriction that reduces blood flow to the disc and to the bone undergoing fusion — precisely the tissues that most need vascularisation in order to heal. At CICOVE, for elective fusions, we require a minimum of six weeks of documented smoking cessation before surgery. This is not arbitrary — it is the difference between a pseudarthrosis rate of 10% and one of 25–40% in active smokers.

Yes, significantly and demonstrably. Poorly controlled diabetes (HbA1c >7.5–8%) increases the risk of surgical wound infection in spine surgery up to threefold; in fusions with implants, the risk is higher still. It compromises vascularisation of the bone graft, delays consolidation of the fusion, and alters dural healing. Perioperative hyperglycaemia (glucose >200 mg/dL in the immediate postoperative period) is an independent predictor of deep infection.

The good news: the risk is modifiable. Preoperative glycaemic optimisation — ideally HbA1c <7.5%, with glucose controlled in the 48 hours before surgery — reduces the risk to levels comparable to a well-controlled non-diabetic patient. The anaesthetist and the surgeon coordinate perioperative glycaemic management; the patient must arrive at surgery with the diabetes well managed.

Intraoperative neurophysiological monitoring (IONM) is the real-time supervision of nervous system function during surgery — through electromyography (EMG), somatosensory evoked potentials (SSEP) and motor evoked potentials (MEP). It detects changes in nerve function and allows the surgeon to adjust technique in the moment.

The evidence supports that IONM significantly reduces the incidence of new postoperative neurological deficits in higher-risk spine surgery. Its use is standard in multilevel fusions, deformity corrections, cervical surgery close to the cord, and any case with distorted anatomy (revisions). The reason we use it in 100% of cases — including relatively straightforward procedures — is that the anatomical distortion left by a previous operation turns any dissection into higher-risk surgery, even when the planned technique is simple. IONM helps identify potentially relevant physiological changes; it does not guarantee that a neurological injury will be avoided.

No. MIS surgery is superior in specific situations: lumbar discectomy in a patient without previous surgery, single-level decompression in stenosis without deformity, single-level fusion in a patient with good anatomy. But not every condition is a candidate for MIS, and the pressure to «do everything endoscopically» is not always backed by evidence.

Open surgery remains the choice in: complex multicolumn deformities, infections requiring extensive debridement, spinal tumours, sagittal deformity corrections, and revisions with dense epidural scarring. In a reoperation, scar tissue eliminates the natural dissection planes that make MIS possible — forcing it in that context can be more dangerous than an open approach. The principle is not which technique looks «more advanced» — it is which technique offers the best balance between access and tissue damage for that specific case.

Fusion adds fixation to decompression when there is real instability, or when the necessary decompression would create it. The criteria with the strongest evidence: demonstrated dynamic instability (more than 4 mm of translation or more than 10° of angulation on flexion-extension), symptomatic spondylolisthesis (supported by the SLIP trial, NEJM), the need to remove more than 50% of a facet joint to decompress adequately, or correction of sagittal deformity requiring rebalancing.

Decompression alone is appropriate when the canal is narrow without dynamic instability, sagittal alignment is correct, and the necessary facetectomy is less than 50% bilaterally. Fusing unnecessarily is an error with permanent consequences: it eliminates motion at that segment, accelerates adjacent degeneration, and can produce the very disease it was meant to treat a few levels higher. Fusion is permanent — the indication must be precise.

This question defines failed back surgery syndrome (FBSS), which affects between 10 and 40% of patients depending on the series and type of surgery. The most frequent causes, in order of probability: (1) incorrect preoperative diagnosis (the pain was not coming from where the surgery was performed), (2) wrong level (L4-L5 was operated and the problem was L5-S1), (3) insufficient decompression, (4) recurrent herniation, (5) epidural fibrosis, (6) pseudarthrosis in fusions, (7) adjacent segment disease, (8) psychosocial factors not identified preoperatively.

Diagnosing FBSS requires revisiting the entire diagnostic process from the beginning — not assuming the previous surgery was correctly indicated. In many cases, the assessment reveals that the cause of failure is identifiable and correctable. In others, treatment is multimodal (pharmacological, rehabilitation, spinal cord stimulation) without further surgery.

Pseudarthrosis is the failure of a spinal fusion to consolidate — the bones do not knit within the expected period (6–12 months for lumbar fusions). The joint that should have been eliminated persists with pathological motion, producing continuous axial pain and a risk of implant fracture. The overall rate is 5–35% depending on the level, the number of segments, and patient factors.

The risk factors with greatest impact: smoking (doubles the rate), poorly controlled diabetes, osteoporosis, chronic corticosteroid use, vitamin D deficiency, and fusion of three or more levels. Diagnosis requires high-resolution CT — MRI is not the study of choice for assessing bony consolidation. Treatment of symptomatic pseudarthrosis is surgical: revision with reinforcement of the fusion and correction of modifiable risk factors.

This distinction has a direct clinical consequence: epidural fibrosis generally has no surgical indication; a recurrent herniation may. MRI without contrast is not sufficient to distinguish them reliably. MRI with intravenous gadolinium is the standard study for this differential diagnosis:

Epidural fibrosis enhances immediately and homogeneously — it has active vascularisation and the inflammatory cells accumulate gadolinium. A recurrent disc herniation does not enhance — disc material is avascular. This signal difference on the post-gadolinium T1 sequence has sensitivity and specificity above 85% for the distinction. At CICOVE, any patient who has had previous surgery and presents with recurrent pain receives a gadolinium MRI as the first diagnostic step — not as an option.

There is no absolute numerical limit, but the results of each successive operation are progressively less predictable. A second lumbar discectomy has results comparable to the first in 70–75% of cases. The third and fourth operations in the same patient have significantly lower success rates and higher risk of complications — dense epidural scarring, distorted anatomy, loss of implant fixation.

What matters more than the number of surgeries: whether the cause of failure is clear and correctable. A pseudarthrosis identified in an L4-S1 fusion with a fractured screw has a specific, correctable cause — revision has a good prognosis even as a third operation. Persistent post-fusion pain with no identifiable structural cause on imaging has no surgical solution, regardless of how many times it is operated. Preoperative assessment in revision surgery matters more than in primary surgery.

Preoperative assessment in revision surgery is more complex and more critical than in primary surgery. Essential steps: (1) Up-to-date gadolinium MRI (distinguishes fibrosis from herniation, assesses current level of compression). (2) High-resolution CT if implants are present (assesses pseudarthrosis, screw position, hardware integrity). (3) Dynamic flexion-extension radiographs (residual instability). (4) Critical review of the operative report from the previous surgery (level operated, technique, intraoperative findings). (5) Formal psychosocial assessment.

The most important question before a reoperation is: is there a clear structural cause, identified on imaging, that explains the current symptoms and is surgically correctable? If the answer is «no» or «perhaps», reoperation has a high probability of producing the same result as the previous one. Being honest about this — even when it is the answer the patient does not want to hear — is part of the work of a revision specialist.

Facet joint pain is axial spinal pain originating in the zygapophysial joints and transmitted by the medial branch of the dorsal ramus. It is characteristically predominantly axial (in the back, not travelling down the leg), worse with extension and trunk rotation, radiating towards the buttock or thigh but not beyond the knee, and relieved by flexion.

Pure discogenic pain is also axial but follows a different pattern, frequently worse with prolonged sitting and on standing up, with a diffuse «fatigue» component. The fundamental problem: no combination of symptoms, physical signs or imaging findings can confirm a facet origin with certainty. The only reliable diagnostic test is a medial branch block that temporarily abolishes the pain — and it must be performed twice, with anaesthetics of different duration, to be valid.

The false-positive rate of a single diagnostic medial branch block is 25–40%. This means that 1 in every 3 or 4 patients who report significant relief from a single block do not in fact have facet pain as the main cause — the relief was a placebo response, systemic anaesthetic effect, or non-specific analgesia.

The two comparative block protocol reduces the false-positive rate to under 5%. A short-acting anaesthetic (lidocaine, 1–2 hours) is used in the first session and a long-acting one (bupivacaine, 3–5 hours) in the second, on different days. The patient must report relief consistent with the expected duration of each agent. This protocol is the single most powerful predictor of rhizotomy outcome. The MINT trial (JAMA 2017) showed null results in part because it required only one block — knowingly admitting up to 40% false positives into the treatment group.

The evidence is solid when patient selection is correct. Lord et al. (N Engl J Med, 1996) — the foundational trial: 24 patients with cervical zygapophysial pain confirmed by two blocks, randomised to real RF versus sham. Median duration of relief: 263 days with real RF versus 8 days with sham. Dreyfuss et al. (Spine, 2000): 60% of patients with lumbar RF had ≥90% pain relief at twelve months.

The MINT trial (Juch et al., JAMA 2017) showed null results, but its methodological flaw is well known: it required only one diagnostic block, admitting 25–40% false positives. Studies with a rigorous two-block protocol consistently confirm the Lord 1996 findings. The honest conclusion: medial branch RF has Level I evidence when patient selection is correct. Without the two blocks, it is a procedure with a high probability of failure.

Laser rhizotomy and conventional RF rhizotomy share the same therapeutic target: thermal ablation of the medial branch nerve. The difference is the energy delivery system (photothermal versus electromagnetic), not the mechanism of action. As of 2026 there is no published randomised controlled trial demonstrating that laser produces superior results to conventional RF for facet pain.

What is available are case series and observational studies with historical comparators — the weakest level of evidence in the hierarchy. Conventional RF has two trials in the New England Journal of Medicine; laser has none of that calibre for this specific indication. Higher cost and technical complexity without support from controlled evidence are not arguments in favour of any medical procedure. A patient offered laser for facet pain should ask which controlled trial supports it.

Yes and yes. The medial branch nerve always regenerates — typically between 6 and 18 months. This is neither a complication nor a failure of the procedure — it is the normal biology of peripheral nerves after thermal ablation. Pain returns when the nerve recovers its transmission function.

The practical implication is favourable: rhizotomy is a repeatable procedure with consistent results across successive cycles — with no evidence of tolerance or of progressively worse outcomes on repetition. MacVicar et al. (2013) documented consistent results across multiple repeated cycles. The correct trigger for repeating the procedure is not a calendar («every 12 months»), but the return of the original pain pattern to its pre-rhizotomy character. Repeating before the nerve has regenerated adds no benefit and adds unnecessary procedures.