‘Yellow Flags’ in Chronic Pain

Role and Relevance in Headache

Recently, the role and relevance of ‘Yellow Flags’ in chronic pain has been questioned.¹

The average length of history of headache/migraine patients presenting to a dedicated headache clinic is 15 years;² these people therefore often present with chronic pain and are depressed, anxious etc.; this is not unreasonable in the presence of constant headache or two-three Migraine episodes a week, or being bed-ridden for 25% of their life.²

Personal psychological variables are not risk factors for chronicity,^3,4 but some consider social factors can be.³ For this reason biopsychosocial reasons are often attributed to ongoing pain. This is exacerbated by the fact that there is no demonstrable pathology in Cervicogenic Headache and unknown pathophysiological processes in Primary Headache.

The biopsychosocial model invites medical ‘nihilism’ – it is easy and convenient to assume that chronic pain is entirely biopsychosocial with no biomedical basis;³ the biopsychosocial concept is prejudicial to chronic pain patients if the pain is attributed, without valid evidence, to biopsychosocial factors, and the cause of pain is ignored or pursued unconvincingly.³ Furthermore, in situations where progress has been disappointing (particularly if the treatment history involves multiple practitioners) it is even more attractive and convenient to focus on the biopsychosocial factors, but this is neither reliable nor valid. There are no objective diagnostic criteria. A psychological diagnosis, to the exclusion of a biomedical one, is no more than an opinion.³

Indeed, ‘Yellow Flags’ and the screening tools employed to identify them need to be critically re-examined by health professionals for their content, in terms of validity and reliability, and the effect their use might have on the client-therapist relationship and clinical reasoning process;¹ focusing on Yellow Flags could result in a diminished service for the patient.¹

In a recent (2017) review,⁵ 27 prospective studies, including prospective cohorts and trials of preventive interventions, predictors, moderators, and mediators of prognosis and outcomes in chronic headache were examined.

The findings suggest with moderate-quality evidence that depression/anxiety, medication overuse, poor sleep, high stress, and higher coping and low headache management self-efficacy (HMSE) are associated with worse outcomes. Lower-quality evidence suggests that higher expectations, age, age at onset, headache frequency, intensity, BMI, disability scores, and employment are potential predictors.⁵

The highest-quality (i.e. moderate-quality) evidence suggests that psychosocial factors, anxiety and mood disorder, sleep and stress, and HMSE are potential prognostic factors. Specifically, groups with low mood (anxiety and mood disorder) appear to respond better to antidepressants and stress management therapy. (Chronic headache patients are usually taking antidepressants or at least have undergone a trial of antidepressants). In the absence of anxiety and mood disorder, (HMSE) improves treatment outcomes. Some evidence suggested that more positive expectations about treatment are associated with better outcomes. However, it was not possible to identify prognostic factors from studies providing high-quality evidence.⁵

Therefore, the review findings:

‘… indicate that the evidence is scarce. No high-quality evidence was provided for any of the potential prognostic factors; therefore, no definite clinical conclusion can be drawn about factors predicting the prognosis of patients living with chronic headache or factors that influence or predict treatment response.’ ^{5; p.299}

Furthermore, research demonstrates that psychological factors are not the main factors responsible for central hyper-excitability i.e., spinal cord hyper-excitability appears to not be affected, at least significantly, by psychological factors,⁶ and… Brainstem sensitisation is the underlying disorder in Migraine, indeed Primary Headache and chronicity in headache generally.^7-12

Despite this context, debate continues as to whether psychological distress precedes and causes chronic pain or, conversely, psychological distress is a consequence of chronic pain.³

However, the literature (and clinical experience) suggests that it is pernicious to focus on biopsychosocial factors in chronic headache; changing patients’ pain by identifying and successful intervention of relevant biomedical sources is the most powerful instrument in effecting changes in lifestyle and perspectives.¹³

The evidence suggests that Yellow Flags are not instrumental in the outcomes of chronic headache patients. Therefore, whilst it is recognised that psychological, behavioural, and lifestyle factors may influence a physical disorder in chronic headache patients at various times,⁴ identifying and managing relevant biomedical disorders should be, and is the focus, thus ensuring the provision of a committed service.³

References:

1. Stewart J, Kempenaar L, Lauchlan D. Rethinking yellow flags. Man Ther. Apr 2011;16(2):196-198.
2. Watson D. Pers. experience 2018.
3. Bogduk N. Whiplash can have lesions. Pain Res Manag. Autumn 2006;11(3):155.
4. Pikoff HB. Psychological mislabeling of chronic pain: lessons from migraine in the 20th century. Pain management. Mar 2017;7(2):127-132.
5. Probyn K, Bowers H, Caldwell F, et al. Prognostic factors for chronic headache: A systematic review. Neurology. Jul 18 2017;89(3):291-301.
6. Sterling M, Hodkinson E, Pettiford C, Souvlis T, Curatolo M. Psychologic factors are related to some sensory pain thresholds but not nociceptive flexion reflex threshold in chronic whiplash. Clin J Pain. Feb 2008;24(2):124-130.
7. Milanov I, Bogdanova D. Trigemino-cervical reflex in patients with headache. Cephalalgia. Feb 2003;23(1):35-38.
8. Nardone R, Ausserer H, Bratti A, et al. Trigemino-cervical reflex abnormalities in patients with migraine and cluster headache. Headache. Apr 2008;48(4):578-585.
9. Katsarava Z, Lehnerdt G, Duda B, Ellrich J, Diener HC, Kaube H. Sensitization of trigeminal nociception specific for migraine but not pain of sinusitis. Neurology. Nov 12 2002;59(9):1450-1453.
10. Katsarava Z, Giffin N, Diener HC, Kaube H. Abnormal habituation of ‘nociceptive’ blink reflex in migraine–evidence for increased excitability of trigeminal nociception. Cephalalgia. Oct 2003;23(8):814-819.
11. Kaube H, Katsarava Z, Przywara S, Drepper J, Ellrich J, Diener HC. Acute migraine headache: possible sensitization of neurons in the spinal trigeminal nucleus? Neurology. Apr 23 2002;58(8):1234-1238.
12. Sandrini G, Proietti Cecchini A, Milanov I, Tassorelli C, Buzzi MG, Nappi G. Electrophysiological evidence for trigeminal neuron sensitization in patients with migraine. Neurosci Lett. Jan 14 2002;317(3):135-138.
13. Wallis BJ, Lord SM, Bogduk N. Resolution of psychological distress of whiplash patients following treatment by radiofrequency neurotomy: a randomised, double-blind, placebo-controlled trial. Pain. Oct 1997;73(1):15-22.