The term “Golden Month” refers to a period of approximately one month following an initiating painful event in which medical intervention is key to preventing the development of chronic pain in high risk patients. High risk patients include those with post-traumatic pain, smokers and patients with anxiety/depression. Confounding factors such as predisposition, expectation and nature of injury are also key to the development of chronic pain.

For example, whiplash injury, though a relatively minor trauma, has been shown to evoke an immune response and is associated with a systemic dysregulation in the number of cells secreting inflammatory cytokines (signalling molecules that mediate and regulate the immune response and inflammation). However, in a country (Lithuania) in which there is little awareness of the possibility of chronic symptoms arising from whiplash, no fear of long term disability and hence zero contact with health services post-whiplash trauma, development of chronic whiplash associated disorder and pain is minimal. In a placebo study in which participants were subject to experimental low-velocity rear-end collisions, subjects who were prone to psychological stress reported whiplash symptoms. Furthermore, a systematic review of 10 studies of 4,700 subjects in total found that patients with acute or subacute pain who had negative expectations about their recover had significantly greater odds of being absent from work at a given time point more than 12 weeks after the onset of pain.

Numerous studies, such as those mentioned above, highlight the importance of compounding psychological factors in the development of chronic pain. Despite this, the medical model foremost recommends physiotherapy, medical imaging and specialist assessments, whilst ignoring psychological intervention, for the treatment of post-traumatic pain.

It is proposed that “Golden Month Treatment” involve the following six modes:

1. Positive expectations of recovery – give the patient facts and fill the information vacuum;
2. Smoking cessation – numerous studies correlate smoking to an increased risk of transitioning to chronic pain;
3. The achievement of an anti-hyperalgesic state - i.e. through restorative sleep, calmness and optimal dietary input (e.g. vitamin D, magnesium, omega-3 fats);
4. Exercise – studies show that increasing exercise 1 week after injury reduces neuropathic pain;
5. Regulated vagal tone - i.e. slow breathing practice / yogic breathing technique – studies show that decreased parasympathetic activation (vagal tone) is implicated in chronic pain. Parasympathetic activity can be increased by slowing the heart rate via slow breathing technique. This can also regulate stress levels;
6. Aggressive multimodal analgesia – beginning with primary care analgesia (i.e. paracetamol and NSAIDs) and moving onto pain clinic analgesia (i.e. opioids, psychotropic medications, interventional treatment) when necessary.

References & Further Reading

1. Kivioja J et al. Systemic immune response in whiplash injury and ankle sprain: elevated IL-6 and IL-10. Clin Immunol 2001; 101:106-12. http://www.ncbi.nlm.nih.gov/pubmed/11580233
2. Obelieniene D et al. Pain after whiplash: a prospective controlled inception cohort study. J Neurol Neurosurg Psychiatry 1999; 66:279-83. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1736255/
3. Castro WH et al. No stress—no whiplash? Prevalence of “whiplash” symptoms following exposure to a placebo rear-end collision. Int J Legal Med 2001; 114:316-22. http://www.ncbi.nlm.nih.gov/pubmed/11508796
4. Hallegraeff JM et al. Expectations about recovery from acute non-specific low back pain predict absence from usual work due to chronic low back pain: a systematic review. J Physiother 2012; 58:165-72. http://www.ncbi.nlm.nih.gov/pubmed/22884183
5. Petre B et al. Smoking increases risk of pain chronification through shared corticostriatal circuitry. Hum Brain Mapp 2015; 36:683-94. http://www.ncbi.nlm.nih.gov/pubmed/25307796
6. López-Álvarez VM et al. Early increasing-intensity treadmill exercise reduces neuropathic pain by preventing nociceptor collateral sprouting and disruption of chloride cotransporters homeostasis after peripheral nerve injury. Pain 2015; 156:1812-25. http://www.ncbi.nlm.nih.gov/pubmed/26090759
7. Detloff MR et al. Acute exercise prevents the development of neuropathic pain and the sprouting of non-peptidergic (GDNF- and artemin-responsive) c-fibers after spinal cord injury. Exp Neurol 2014; 255:38-48. http://www.ncbi.nlm.nih.gov/pubmed/24560714
8. Shankarappa SA et al. Forced-exercise delays neuropathic pain in experimental diabetes: effects on voltage-activated calcium channels. J Neurochem 2011; 118:224-36. http://www.ncbi.nlm.nih.gov/pubmed/21554321
9. Stagg NJ et al. Regular exercise reverses sensory hypersensitivity in a rat neuropathic pain model: role of endogenous opioids. Anaesthesiology 2011; 114:940-8. http://www.ncbi.nlm.nih.gov/pubmed/21386701
10. Tracy LM et al. Meta-analytic evidence for decreased heart rate variability in chronic pain implicating parasympathetic nervous system dysregulation. Pain 2016; 157:7-29. http://www.ncbi.nlm.nih.gov/pubmed/26431423
11. Image: Emergency image, 2010, viewed 18 November 2015, http://sonamba.com/the-golden-hour-and-rapid-response.