Abstract
In patients with multiple sclerosis (MS), pain is a frequent and disabling symptom. The prevalence is in the range 29–86 % depending upon the assessment protocols utilised and the definition of pain applied. Neuropathic pain that develops secondary to demyelination, neuroinflammation and axonal damage in the central nervous system is the most distressing and difficult type of pain to treat. Although dysaesthetic extremity pain, L’hermitte’s sign and trigeminal neuralgia are the most common neuropathic pain conditions reported by patients with MS, research directed at gaining insight into the complex mechanisms underpinning the pathobiology of MS-associated neuropathic pain is in its relative infancy. By contrast, there is a wealth of knowledge on the neurobiology of neuropathic pain induced by peripheral nerve injury. To date, the majority of research in the MS field has used rodent models of experimental autoimmune encephalomyelitis (EAE) as these models have many clinical and neuropathological features in common with those observed in patients with MS. However, it is only relatively recently that EAE-rodents have been utilised to investigate the mechanisms contributing to the development and maintenance of MS-associated central neuropathic pain. Importantly, EAE-rodent models exhibit pro-nociceptive behaviours predominantly in the lower extremities (tail and hindlimbs) as seen clinically in patients with MS-neuropathic pain. Herein, we review research to date on the pathophysiological mechanisms underpinning MS-associated neuropathic pain as well as the pharmacological management of this condition. We also identify knowledge gaps to guide future research in this important field.
Highlights
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) resulting in motor, sensory and cognitive impairment (Compston and Coles 2008)
L’hermitte’s sign and trigeminal neuralgia are the most common neuropathic pain conditions reported by patients with multiple sclerosis (MS), research directed at gaining insight into the complex mechanisms underpinning the pathobiology of MS-associated neuropathic pain is in its relative infancy
A contributing factor is that treatment evidence, derived from clinical trials of analgesic and adjuvant agents for the relief of MS-associated neuropathic pain to date, is limited by the open-label design, low patient numbers and the relatively short clinical trial duration (Table 1)
Summary
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) resulting in motor, sensory and cognitive impairment (Compston and Coles 2008). Neuropathic pain associated with MS is inadequately relieved or not relieved at all with conventional analgesics such as non-steroidal anti-inflammatory drugs or opioid analgesics such as morphine (O’Connor et al 2008; Kalman et al 2002; Truini et al 2011). We have reviewed research on the most common MS-related neuropathic pain conditions including ongoing pain in the extremities (dysaesthetic extremity pain), as well as paroxysmal pain (trigeminal neuralgia and L’hermitte’s phenomenon) (O’Connor et al 2008; Truini et al 2013). Classic TN and MSassociated TN are both characterised by pain, more frequent sensory deficits and occasional bilateral pain that occur in 20 and 7 % of patients, respectively, are useful criteria for differentiating MS-associated TN from classical neuralgia (Truini et al 2011; Cruccu et al 2008)
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