Clinical synthesis based on the official position of the Bárány Society 2022, the De Vestel 2022 and Carrasco-Uribarren 2025 meta-analyses, the Paquin 2022 critique of the CFRT and the 2023 empirical data on the JPSE (AlDahas).

Dizziness of cervical origin, or cervicogenic dizziness (CGD), is a clinical entity whose nosological status is actively debated. The official position of the Bárány Society 2022 clarifies the framework: it is a non-specific symptom (and not a pathology in itself) defined as imbalance, unsteadiness or light-headedness directly associated with neck movements or positions, in the absence of any other identifiable cause.¹ 🧐

How is this condition defined, who does it affect and what are the risk factors?

The operational definition adopted by most authors rests on three converging criteria.¹٬²٬³ First, vestibular symptoms that are non-specific (unsteadiness, “floating head”, imbalance) rather than true rotatory vertigo. Second, a clear temporal correlation with neck pain or stiffness. Third, the documented exclusion of other causes (BPPV, vestibular migraine, vestibular neuritis, Ménière's, VBI). The verified 2021-2023 epidemiology confirms a high prevalence of dizziness in patients with chronic neck pain. The Norwegian cohort Knapstad 2023 (n = 133) reports 43 % concomitant dizziness in patients with persistent neck pain.⁴ The multicentre Turkish cohort Vural 2021 (n = 2,361) finds a prevalence of 40.1 %.⁵ In patients with whiplash-associated disorders (WAD), up to 70 % report dizziness in the chronic phase according to Treleaven 2017.⁶ In specialist ENT care, however, CGD accounts for only 5-6 % of consultations for dizziness (Frontiers Neurol 2025 perspective).⁷

Risk factors are multiple and interact 🧐 :

• Whiplash-type cervical trauma : the best established. The Treleaven 2017 meta-analysis confirms a persistent prevalence of dizziness in the chronic phase (up to 70 %) with marked proprioceptive deficits, oculomotor disturbances and impaired sensorimotor control.⁶
• Cervical spondylosis and degenerative conditions of the upper cervical spine, particularly the C1-C3 segments (Devaraja 2018, reviewed in Eur Arch Otorhinolaryngol).⁸
• Chronic suboccipital muscle tension and masticatory / suboccipital trigger points (Sung 2020).⁹
• Prolonged postures (screen work, forward head position): the Moustafa 2017 RCT demonstrates that an 8-week postural correction programme significantly reduces dizziness and cervicocephalic kinaesthetic sensibility at 1-year follow-up.¹⁰

What happens in the body and how does cervicogenic dizziness naturally evolve?

The main accepted mechanism is a sensory conflict. 🧠 The upper cervical spine (C0-C3) is densely innervated by mechanoreceptors (neuromuscular spindles, Golgi tendon organs, joint receptors) whose afferents converge on the vestibular nuclei and the cerebellum.⁷ A dysfunction (post-traumatic, inflammatory or degenerative) generates proprioceptive signals incoherent with those of the vestibular and visual systems, producing a sensation of instability.¹¹٬¹² An alternative theory implicates a vascular compression of the vertebral artery during extreme rotations (vertebrobasilar insufficiency). The 2025 systematic review of atherosclerotic VBI confirms that dizziness is the most frequent symptom (27.7 %), but that Coman's classic “5D” (Dizziness, Diplopia, Dysarthria, Dysphagia, Drop attacks) cover only 22 % of the reported features: their isolated predictive value is limited.¹³ The natural course is variable. Without intervention, symptoms can become chronic and fluctuating, with periods of remission and exacerbation triggered by neck movements or sustained postures. With appropriate physiotherapy management, the prognosis is generally favourable in the short and medium term: the De Vestel 2022 meta-analysis (13 RCTs, n = 898) confirms a significant effect on the DHI and the dizziness VAS.¹⁴

In the absence of a gold standard, the diagnosis of CGD rests on a structured approach combining a targeted history, a systematic clinical examination and rigorous exclusion of differential diagnoses.¹ The Bárány Society 2022 stresses that no single test is sufficient, and that “proof by treatment” (diagnosis confirmed retrospectively by the therapeutic response) remains pragmatic but scientifically weak.¹

Which questions should you ask to understand the patient and their history?

The history aims to establish the plausibility of the cervico-vestibular link.²

• Timing : did the dizziness begin at the same time as, or after, the onset of the neck pain / of a neck trauma? This correlation is essential.
• Description of the symptom : unsteadiness, “floating head” (light-headedness) or imbalance. True rotatory vertigo (“the room is spinning”) should raise suspicion of a peripheral or central vestibular cause.
• Triggers : neck rotation / extension movements, sustained postures. A purely positional trigger (lying down, getting up) points rather to BPPV.
• Past history : whiplash injury, cervical surgery, known osteoarthritis, previous vestibular comorbidities.
• Associated symptoms : headaches, visual disturbances, tinnitus, aural fullness (Ménière's?), nausea, photophobia (vestibular migraine?).

Vascular reasoning, before any cervical intervention

This population is precisely the one that exposes the physiotherapist: the IFOMPT international cervical framework, published in JOSPT in 2023, points out that dizziness is present in 32 % of arterial dissections and in 20 % of vertebrobasilar dissections.¹⁶ In other words, the reason for consultation may be the first sign of the very pathology one is about to mobilise. This framework therefore asks that vascular reasoning be carried out before any intervention on the cervical spine, mobilisations and exercise included, and not only on the eve of a manipulation. Three points in it change practice.

• Pre-manipulative positional tests are removed from the framework. Sustained rotation-extension positioning intended to “test the vertebral artery” is no longer recommended: its predictive capacity is lacking, and a negative test has never reassured about anything other than itself.¹⁶
• What replaces them is a cluster, not a test. History oriented towards cardiovascular risk factors and towards the unusual nature of the headache or neck pain, measurement of blood pressure, examination of the cranial nerves and neurological examination, observation of the gait pattern, then informed consent obtained in full knowledge of the risk.¹⁶
• The vocabulary changes because the reasoning changes. We speak of vascular pathologies of the neck, and no longer of “vertebrobasilar insufficiency” or “cervical arterial dysfunction”. These labels designated an entity to be confirmed before authorising the procedure; the clinical question posed by the framework is different: is the intended intervention safe for this patient, today?¹⁶

The “5D-3N” keep their place in the list of red flags above, but for what they are: late and poorly specific signs, of which the five Ds cover only 22 % of the manifestations reported in the 2025 systematic review.¹³ They are not the filter to apply before mobilising or manipulating. There remains the limit of the framework itself, which must be known so as not to replace one false sense of security with another. Tested, in the Dutch project Go4Safe, against a consensus medical decision made by a vascular neurologist and an interventional neurologist with neuroradiological opinion and cervical MR angiography, it obtains a sensitivity of 0.50, with a specificity of 0.63 and an AUC of 0.57.¹⁷ A negative screening therefore does not allow the conclusion that the vascular side is ruled out: the framework structures and documents the decision, it does not give a green light.

Which clinical tests should be carried out and which other conditions need to be ruled out?

The clinical examination combines two complementary approaches: (1) reproducing the symptoms through cervical loading, and (2) actively excluding the vestibular causes.

Cervical orienting tests

• Cervical Flexion-Rotation Test (CFRT) : normal range ≈ 44° to each side in maximal cervical flexion; positive threshold < 32° or a difference ≥ 10° between sides.³ Beware of the origin of these figures: the sensitivity of 91 % and the specificity of 90 % come from the original 2007 study by Ogince, conducted in patients with cervicogenic headache of C1-C2 origin, and have never been established for cervicogenic dizziness (Hall 2010, also in a headache population, reports 75 % and 92 %). These diagnostic properties are moreover probably overestimated according to the Paquin 2022 critical analysis (imperfect gold standard, inclusion bias).⁴
• Joint Position Sense Error (JPSE) : the historical threshold of Revel 1991 was > 4.5°. The recent empirical data from AlDahas 2023 (n = 43) show that healthy subjects have on average 2-2.5° of error, and patients with chronic neck pain 3.5-4.8°: a clinical threshold of 3-4° offers a better sensitivity/specificity compromise.⁵٬⁶
• Head-Neck Differentiation Test (HNDT) and Smooth Pursuit Neck Torsion Test (SPNT) : reproduction of symptoms by trunk rotation with the head fixed, which points to a cervical origin (L'Heureux-Lebeau 2014).⁷
• Segmental palpation C0-C3, active and passive joint mobility, search for suboccipital and upper trapezius trigger points.

Mandatory differential diagnosis (in order of frequency)

🎯 As the diagnosis of CGD is a diagnosis of exclusion, it is essential to test for and eliminate the most frequent causes of dizziness:

This prioritisation follows the ICD-11 criteria (MB48 Dizziness or giddiness, AB31.7 Vertiginous syndromes, AB32.0 PPPD) and the Bárány Society 2022 position.¹٬⁸٬⁹٬¹⁰

Should patients with cervicogenic dizziness be classified, and for what benefit?

The classification is still under development but clinically useful. The Bárány Society 2022 consensus distinguishes two levels of diagnostic certainty:

• “Probable” cervical dizziness : criteria fulfilled with a plausible temporal correlation.
• “Definite” cervical dizziness : confirmed retrospectively by the disappearance of symptoms after treatment of the cervical dysfunction.

A clinical stratification according to the presumed mechanisms can guide treatment:

• Traumatic profile (post-WAD): marked proprioceptive deficits, oculomotor disturbances, impaired sensorimotor control. Therapeutic target: proprioceptive + oculomotor rehabilitation (Treleaven 2017, Sterling 2004).¹¹٬¹²
• Degenerative profile (cervical spondylosis): C1-C3 joint restriction, mechanical pain. Target: gentle manual therapy + mobility + endurance.
• Functional profile (muscular / postural): trigger points, forward head posture. Target: myofascial release, postural correction, strengthening.

Critique and controversy

The diagnosis of CGD remains a diagnosis of exclusion without a pathognomonic test. The Bárány 2022 position stresses that no isolated sign or test is sufficient, and that “proof by treatment” is pragmatic but scientifically weak. The Paquin 2022 critical analysis warns that the CFRT, often presented as a reference test, has its diagnostic properties probably overestimated by inclusion biases and the imperfection of the gold standard used (manual examination). A rarely stated limit must be added: the values usually put forward (sensitivity 91 % / specificity 90 %, Ogince 2007) were obtained in cervicogenic headache of C1-C2 origin, and not in cervicogenic dizziness, where the test has no established diagnostic properties. The clinician should therefore regard these tests as orienting elements within a cluster of arguments, not as verdicts. Another controversy concerns the real weight of cervical afferents in overall balance : their role is anatomically proven, but the extent of their contribution relative to the vestibular and visual systems remains debated.

Treleaven (2024) proposes, rather than deciding for or against cervicogenic dizziness, to assess the neck's share in the dizziness (none, comorbid, minor, major or compensatory), because mixed presentations are frequent. This is an expert proposal, not validated, which does not remove the need to look for central, vascular and vestibular causes.¹⁸

The 2022-2025 literature converges on a multimodal approach combining manual therapy, targeted exercise and patient education.¹ 💡 However, levels of evidence remain low to very low according to GRADE, and the optimal dose is not established.

Where do you start? What is the recommended hierarchy of interventions?

The De Vestel 2022 meta-analysis remains the most solid reference to date: 13 RCTs included, n = 898 patients.¹ 🩺 The mean effects (mean differences) are as follows:

• Dizziness intensity (VAS) : MD = −22.56 [95 % CI −28.11; −17.01], p < 0.001, I² = 0 %.
• DHI : MD = −10.04 [95 % CI −16.36; −3.73], p = 0.002, I² = 79 % (high heterogeneity).
• CROM flexion-extension : MD = +7.18° [95 % CI 3.65; 10.70].
• Neck pain VAS : MD = −14.01 [95 % CI −22.77; −5.26].

GRADE level of evidence : De Vestel 2022 rated as moderate the certainty for manual therapy alone; very low for the combination of manual therapy + exercise (stronger effect but lower quality of evidence).¹ The more recent meta-analysis by Carrasco-Uribarren 2025 (6 primary RCTs, n = 272) points in the same direction for upper cervical interventions on the DHI (MD −7.30) and the dizziness VAS (MD −19.34), with a GRADE certainty rated low to very low.²

What is the place of exercise, and is there a superior approach?

Exercise is not optional, but no protocol has demonstrated absolute superiority. Personalisation takes precedence over format. 🏋️‍♂️ Three categories of exercise are validated:

• Sensorimotor control and proprioception : joint repositioning with a laser pointer, target tracking, oculomotor exercises coordinated with cervical movement. This is the most direct target of the pathophysiological mechanism (Lystad 2011).³
• Vestibular and oculomotor rehabilitation : eye fixation exercises during head movements (VOR x1, x2), saccades, habituation. The RCT by Piromchai 2023 (n = 68) shows a significant reduction in the DHI at 2 weeks with a home self-exercise programme.⁴
• Strengthening and endurance : deep neck flexors (longus colli) and scapular stabilisers. Moustafa 2017 showed that an 8-week postural correction programme improves alignment and reduces the intensity of dizziness.⁵

Manual therapies, technologies: how effective are they really?

Manual interventions are the most studied and offer the most solid quantitative data in the field. 🤲 Before indicating them in a patient who consults for dizziness, one step is non-negotiable: the vascular reasoning of the IFOMPT 2023 cervical framework, carried out before any intervention on the cervical spine and not only on the eve of a manipulation, since mobilisations and exercise explicitly fall within its scope.¹³ In practice (details in chapter 2): history of cardiovascular risk factors and of the unusual nature of the headache or neck pain, blood pressure, examination of the cranial nerves and neurological examination, then informed consent, pre-manipulative positional tests no longer being recommended. This reasoning documents the decision without ever guaranteeing it: against a consensus medical decision made by a vascular neurologist and an interventional neurologist, with cervical MR angiography as support, the framework shows a sensitivity of 0.50, a specificity of 0.63 and an AUC of 0.57.¹⁴ A negative screening therefore does not allow the conclusion that the vascular risk is ruled out, and monitoring of symptoms remains in order during and after the session.

• Upper cervical mobilisations (Maitland techniques, Mulligan SNAGs): the placebo-controlled trial Reid 2014 (n = 86, Phys Ther, therapist not blinded) finds SNAGs and Maitland comparable, both better than placebo on dizziness intensity and frequency at 12 weeks; the DHI improves in all three groups.⁶ At 12 months (Reid 2015), the advantage over placebo persists for dizziness frequency, the DHI and global perceived effect, but not for dizziness intensity or pain: a single trial.⁷
• Soft tissue techniques : inhibition of the suboccipitals, myofascial release. Promising data but small trials (n typically < 50).
• Mechanisms : Bialosky 2018 (JOSPT) proposes an integrated model: peripheral, spinal and supraspinal neurophysiological effects, modulated by patient expectations and the therapeutic alliance.⁸

Beyond the physical: how can we educate the patient and address psychological factors?

Anxiety is a major factor in vestibular disorders. The meta-analysis Kim 2026 (n = 764,403) shows a prevalence of anxiety of 30.6 % in BPPV patients, 47.0 % in Ménière's patients and 46.5 % in vestibular migraine.⁹ The PPPD (ICD-11 AB32.0) can develop secondarily after any vestibular episode in 15-20 % of patients.¹⁰ 🧠 Therapeutic education has three aims: (1) explaining the mechanism of the reversible sensory conflict (no “danger” to the spinal cord or the brain); (2) reassuring without minimising (real symptoms but with a favourable prognosis under management); (3) giving self-management tools (simple home exercises, management of acute episodes, identification of triggers).¹¹ The screening for anxiety and catastrophising (PCS, GAD-7, HADS) is recommended because these factors predict chronicity and non-response to treatment.¹²

Critique and controversy

The CGD field suffers from three persistent methodological weaknesses :

1. Absence of a diagnostic gold standard : the populations included in the RCTs are heterogeneous, which explains the high I² (up to 79 % for the DHI in De Vestel 2022).
2. Placebo effect and therapeutic alliance not separated : manual therapy involves physical contact and sustained attention. The specific vs non-specific share of the effect remains unknown (Bialosky 2018).
3. Rare long-term follow-up : are the benefits observed at 4-12 weeks maintained at 1 year? Reid 2015 finds, against placebo, an advantage at 1 year on dizziness frequency and the DHI, but not on its intensity: a single trial.

The post-acute phase is crucial. In the placebo-controlled trial by Reid 2015, both manual therapies keep an advantage at 12 months for dizziness frequency, the DHI and global perceived effect, but not for dizziness intensity or pain.¹ Empowering the patient to manage their residual symptoms remains the goal of this phase.

How can self-management make the patient an active participant in their own recovery?

Self-management rests on two pillars: therapeutic education and home exercise programme. 🧠 Essential components validated by Piromchai 2023 (RCT n = 68):²

• Proprioception and motor control : slow active repositioning (10-15 repetitions, 2x/day), with visual feedback (laser on a cap or headband).
• Cervical stabilisation : isometrics of the deep flexors (cranio-cervical flexion test, 10 sec × 10 repetitions, progression over 4-6 weeks).
• Vestibular and oculomotor rehabilitation : VOR x1 / x2 (10 cycles, progressive increase in speed), horizontal and vertical saccades.
• Self-mobilisations : SNAGs (Mulligan) in cervical rotation, static suboccipital stretches.

Therapeutic education must explicitly address the reversible nature of the sensory conflict, the absence of serious underlying pathology (once red flags have been ruled out), the management of acute episodes and the identified triggers (postures, stress, fatigue).

When and how should a safe return to sport and activities be planned?

No standardised protocol exists specifically for CGD. Progression should follow the general principles of return to sport (RTS) after neck pain + concussion, in particular for contact sports or post-WAD athletes.³٬⁴ 💪 In the concussed athlete whose dizziness, neck pain or headaches persist beyond 10 days, the Amsterdam 2022 consensus endorses individualised cervico-vestibular rehabilitation, which could shorten the time to return to sport compared with rest followed by graded exertion (systematic review, few trials).⁸٬⁹

Prerequisites before starting the progression :

1. No dizziness at rest or during activities of daily living.
2. Full, pain-free cervical ROM.
3. Normalised sensorimotor control tests (JPSE < 3°, balance on foam with eyes closed > 30 sec).
4. NDI < 10/50, DHI < 30/100.

Critique and controversy

The uncertainty about the specificity of the interventions remains. Trials show that manual therapy alone improves symptoms in the short term, but that the combination with exercise is necessary for durability. This suggests that the maintenance of results depends less on the initial manual technique than on the active engagement of the patient. The challenge is therefore less technical than behavioural. The prognostic factors of non-response identified by Knapstad 2023 (severe initial neck pain, high NDI, anxious comorbidity, symptom duration > 6 months) should prompt more intensive treatment and early multidisciplinary referral.⁵

Scientific integrity note : the three clinical cases presented below are real publications that can be verified on PubMed/PMC. 🧐 For this article, we reference exclusively PMC / PubMed-verified case reports in open access; no case has been reconstructed or simplified.

Typical case: 38-year-old woman (Minguez-Zuazo 2016, PMC4934967)

The case series by Minguez-Zuazo and colleagues 2016, published in the Journal of Exercise Rehabilitation in open access, describes 7 patients (5 women, 2 men, mean age 38.4 years) with CGD for 28 months on average.¹ The initial pain NRS was 6.29/10.

Protocol: 8 sessions over 4 weeks (twice weekly) :

• Sessions 1-4 : pain education + cervical mobilisations + motor control retraining (cranio-cervical flexion test).
• Sessions 5-8 : progression to endurance strengthening + oculomotor and gaze stability exercises.

This “average” profile illustrates the most common typology in practice: middle-aged female patients, moderate chronic symptoms, responding to a standardised multimodal approach. The large reduction in catastrophising (d = 1.60) suggests that the “education + mobilisations” effect also acts on the cognitive dimension of pain.

The diagnostic challenge: when CGD mimics Ménière's disease (Chu 2021, PMC8577610)

Chu and colleagues 2021 (Journal of Medical Cases, free full text) report the case of a radio presenter aged 40 years, presenting for 12 months with episodic rotatory vertigo + aural fullness + tinnitus + sudden hearing loss in the right ear.² 🤔 The triad suggested Ménière's disease.

Initial diagnosis and treatment failure :

• ENT diagnosis: Ménière's disease.
• Drug treatment for 4 months (betahistine + low-sodium diet + vestibular rehabilitation): complete failure.
• Vestibular and neurological examinations: normal (atypical for Ménière's disease in the active phase).

Cervical reassessment :

• ROM restriction: extension 40/70°, rotation 60/90°.
• Dynamic radiographs: dissociated clivo-axial angle suggesting craniocervical instability.
• Brain MRI: normal.
• Symptom triggers: cervical rotation, eye closure, smartphone.

Treatment : spinal manipulation + intermittent motorised traction + ultrasound, 3 sessions / week for 3 months. Complete resolution at 12 months with radiographic normalisation. This case perfectly illustrates the “mimic” potential of CGD. The negativity of the vestibular tests and the reproduction of symptoms by cervical loading are the key clues. Any dizziness resistant to well-conducted vestibular treatment deserves a cervical reassessment.

Study of a complex case: post-concussion (Teare-Ketter 2021, PMC7872469)

Teare-Ketter and colleagues 2021 (Int J Sports Phys Ther, free full text) describe a patient aged 21 years assessed 356 days after a fall from a golf cart, with impact on the left shoulder and neck.³ Loss of consciousness, post-traumatic amnesia, non-operated left temporal fracture. No follow-up after the emergency care.

Persistent symptoms 12 months later : neck pain, bilateral radicular pain, an inebriated feeling, nausea, dizziness, blurred vision, diplopia, photophobia, balance disorders, headaches triggered by reading and neck movements. Initial RPQ: 20/64.

Clinical assessment : cervical ROM and accessory mobility impaired, abnormal VOR, Fukuda Step Test at 70° of rotation to the left (latent vestibular deficit), abnormal m-CTSIB.

Protocol: 8 sessions of 60 min over 5 weeks, combining: (1) manual therapy (joint mobilisations, soft tissue techniques, neural glides), (2) vestibular rehabilitation (VOR adaptation, saccades, habituation), (3) neuromotor retraining with a laser harness (cervical proprioception).

Results : cervical ROM normalised (except residual left rotation), m-CTSIB and Fukuda Step Test normalised, RPQ: 20/64 → 2/64 (near-complete resolution), occasional mild residual headaches. Post-traumatic cervical dysfunction can persist for 12 months or more in the absence of management. The dual mechanism (concussion + whiplash) justifies systematic cervical assessment of any prolonged post-concussion syndrome, as stressed by Marshall 2015 and the systematic review by Cheever 2021.⁴٬⁵

Critique and controversy

🧠 Clinical cases have a low evidential value in the GRADE pyramid (very low / Oxford CEBM level 4). A single case illustrates a possibility, not a generality. No cause-and-effect relationship can be asserted, because placebo effects, regression to the mean and natural history are not controlled. Published cases also tend to report successes (publication bias). They remain valuable for documenting the existence of atypical presentations (mimicking Ménière's), demonstrating the mechanistic plausibility of cervical management, and generating testable hypotheses.

Applying research-based recommendations requires knowing what to do, when to collaborate and how to measure the impact. 🧑‍⚕️

When and to which other healthcare professionals should patients be referred?

The identification of red flags (see the box in chapter 2) is the first non-negotiable step. The Finucane 2020 international framework (JOSPT) stresses that many traditional red flags have low diagnostic accuracy in isolation and must be interpreted in the context of a complete examination.¹ Beyond emergencies, the presence of yellow flags (catastrophising, kinesiophobia, anxiety, depression) predicts chronicity. The prevalence of anxiety in vestibular patients reaches 30-47 % depending on the condition (Kim 2026 meta-analysis, n = 764,403).² Referral to a clinical psychologist trained in cognitive behavioural therapies is indicated if HADS-A ≥ 11, PCS > 30, TSK ≥ 37, or PHQ-9 > 10.

The structured interprofessional collaboration is central. The physiotherapist, often on the front line, plays a triage role. Clear communication and defined referral protocols with ENT, neurologists and psychologists optimise the care pathway.

How do you measure outcomes and overcome barriers to implementation?

The systematic use of Patient-Reported Outcome Measures (PROMs) is now a quality standard. 📈 For CGD, three tools are essential:

Recommended practice: assess DHI + NDI + dizziness NRS + neck pain NRS at each key consultation (baseline, 4 wk, 8 wk, 12 wk, 6 months). A patient symptom diary usefully complements these PROMs. The knowledge ↔ practice gap is documented: the systematic review Scurlock-Evans 2014 identifies three major barriers to the implementation of EBP in physiotherapy: lack of time, lack of critical appraisal skills, lack of organisational support.³ Effective strategies: in-practice journal clubs, pre-appraised resources (PEDro, Cochrane), peer mentoring.

Critique and controversies: beyond the guidelines

First, the tension between standardisation and personalisation. Practice guidelines are based on population averages. Each patient is unique. Greenhalgh 2014 (BMJ) warned of the “crisis of EBM”: rigid application of protocols can harm the therapeutic alliance, a factor nonetheless essential to achieving good results; Ferreira 2013 quantified this effect in chronic low back pain.⁴٬⁵

Second, the focus on PROMs can obscure other aspects of recovery (subjective quality of life, return to valued activities) and data collection must not come at the expense of listening time.

Third, equity of access to the recommended referrals (psychologist, neurologist, ENT) is highly variable from one area to another. The physiotherapist often ends up on the front line managing the complexity, which highlights the structural limits of the healthcare system more than those of individual practice.