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:
- Positive expectations of recovery – give the patient facts and fill the information vacuum;
- Smoking cessation – numerous studies correlate smoking to an increased risk of transitioning to chronic pain;
- 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);
- Exercise – studies show that increasing exercise 1 week after injury reduces neuropathic pain;
- 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;
- 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
- 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
- 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/
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- Image: Emergency image, 2010, viewed 18 November 2015, http://sonamba.com/the-golden-hour-and-rapid-response.