Key clinical highlights
- Up to 70% of patients with a spinal cord injury (SCI) will develop central neuropathic pain.1
- Despite a loss of mobility, patients with a SCI report pain as being amongst their primary concerns.2
- Neuronal hyperexcitability (central sensitisation) is believed to contribute to central neuropathic pain following a SCI.1,3,4
- It is important to identify patients who may have a neuropathic component to their pain early, as neuropathic pain requires a different therapeutic approach compared to nociceptive pain, and early diagnosis and appropriate management of neuropathic pain may improve health-related outcomes.5
- Screening tools such as the DN4 questionnaire be useful in identifying patients who may have a neuropathic component to their pain.6
It has been estimated that approximately two thirds to 70% of patients with a SCI will develop central neuropathic pain following the injury.1,2
Although loss of mobility is often considered the most serious consequence of a SCI, patients who develop pain following a SCI consistently rate pain as one of the most difficult problems that interferes with their daily life.2
Pathophysiology of central neuropathic pain in SCI
Current understanding of the mechanisms underlying central neuropathic pain in SCI remains incomplete.2
However, neuronal hyperexcitability (central sensitisation) is believed to play a role in its pathophysiology:1,3,4
- Traumatic spinal cord injuries can directly and indirectly produce anatomical and neurochemical changes in the spinal dorsal horn.1
- These changes can lead to maladaptive synaptic circuits and hyperexcitable neurons.
- These hyperexcitable neurons are characterised by:
- A lowered threshold for activation;
- An increased peripheral receptive field size; and
- Increased after-discharge activity.1
Central sensitisation is believed to play an important role in the symptoms of central neuropathic pain (Figure 1).1
Figure 1: Stimulus-response relationship in central sensitisation. Allodynia; a painful response to a normally
non-painful stimuli. Hyperalgesia; increased responsiveness to painful stimuli.7
Location and description
Patients with a SCI may experience pain of varying aetiologies including muscle spasm, spasticity, muscle overuse, mechanical instability of the spine, and neuropathic pain related to spinal cord or nerve root injury.8
The most common types of neuropathic pain associated with SCI are at-level and below-level pain (Table 1).8
Patients with central neuropathic pain may present with sensory alterations, such as:
- Hyperalgesia - an exaggerated pain behaviour evoked by noxious stimuli;9
- Allodynia - pain behavior evoked by non-noxious stimuli;9
- Negative sensory signs – such as numbness;3,4 and
- Spontaneous pain.3
Patients may also exhibit “wind-up” (also called temporal summation or hyperpathia). Which is characterised by an abnormally painful reaction to a repetitive stimulus (e.g. a repetitive pinprick). Wind-up may manifest as an explosive increase in pain severity and/or an increased area of pain.9
As with all neuropathic pain conditions, it is important to identify patients with a neuropathic component to their pain early, as neuropathic pain requires a different therapeutic approach to nociceptive pain. Furthermore, initiating an appropriate intervention early may be associated with better health outcomes for patients.5
Clinical Tip: screening for neuropathic pain
The DN4 is a clinically validated screening tool that can help identify patients who may have a neuropathic component to their pain.6
Click here to learn more and download a free copy.
Links and resources
Patient information sheets
Chronic Pain Australia
Australia’s peak non-profit organisation for chronic pain. Dedicated to reducing the social and other barriers to living with chronic pain.
Spinal Cord Injuries Australia
Dedicated to promoting independence amongst people living with spinal cord injuries
Spinal Injuries Australia
A not-for-profit, membership-based organisation, dedicated to enhancing the lives of people with a spinal injury.
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- Gwak YS & Hulsebosch CE. Neuropharmacol. 2011; 60: 799–808.
- Wrigley PJ, et al. Pain. 2009; 141: 52-59.
- Yezierski RP. Neurosignals. 2005; 14: 182–193.
- Hulsebosch CE, et al. Brain Res Rev. 2009; 60: 202–213.
- Haanpää ML, et al. Am J Med. 2009; 122 (10 Suppl): S13-21.
- Bouhassira D, et al. Pain. 2005; 114: 29-36.
- Costigan M, et al. Annu Rev Neurosci. 2009; 32: 1-32.
- Simpson DM, McArthur JC, Dworkin RH. Neuropathic Pain: Mechanisms, Diagnosis and Treatment. Oxford University Press; 2012.
- Neurology Expert Group. Therapeutic Guidelines: Neurology, 2011 Version 3. Melbourne: Therapeutic Guidelines Limited; 2011.