Abstract
Recurrent myelitis is one of the predominant characteristics in patients with neuromyelitis optica (NMO). While paresis, visual loss, sensory deficits, and bladder dysfunction are well known symptoms in NMO patients, pain has been recognized only recently as another key symptom of the disease. Although spinal cord inflammation is a defining aspect of neuromyelitis, there is an almost complete lack of data on altered somatosensory function, including pain. Therefore, eleven consecutive patients with NMO were investigated regarding the presence and clinical characteristics of pain. All patients were examined clinically as well as by Quantitative Sensory Testing (QST) following the protocol of the German Research Network on Neuropathic Pain (DFNS). Additionally, plasma endocannabinoid levels and signs of chronic stress and depression were determined. Almost all patients (10/11) suffered from NMO-associated neuropathic pain for the last three months, and 8 out of 11 patients indicated relevant pain at the time of examination. Symptoms of neuropathic pain were reported in the vast majority of patients with NMO. Psychological testing revealed signs of marked depression. Compared to age and gender-matched healthy controls, QST revealed pronounced mechanical and thermal sensory loss, strongly correlated to ongoing pain suggesting the presence of deafferentation-induced neuropathic pain. Thermal hyperalgesia correlated to MRI-verified signs of spinal cord lesion. Heat hyperalgesia was highly correlated to the time since last relapse of NMO. Patients with NMO exhibited significant mechanical and thermal dysesthesia, namely dynamic mechanical allodynia and paradoxical heat sensation. Moreover, they presented frequently with either abnormal mechanical hypoalgesia or hyperalgesia, which depended significantly on plasma levels of the endogenous cannabinoid 2-arachidonoylglycerole (2-AG). These data emphasize the high prevalence of neuropathic pain and hyperalgesia in patients with NMO. The degree of mechanical hyperalgesia reflecting central sensitization of nociceptive pathways seems to be controlled by the major brain endocannabinoid 2-AG.
Highlights
Neuromyelitis optica (NMO; Devic’s disease) is a demyelinating inflammatory autoimmune disease of the central nervous system leading to recurrent optic neuritis (ON) and episodic myelitis [1,2,3]
The only patient who did not suffer from central pain within the last three months had an episode of severe definite neuropathic pain during myelitis two years earlier, which was temporarily treated with gabapentin and recovered completely during the following months
Pain has recently been described as another key symptom of NMO, but the predominant quality of pain has not yet been characterized [10,11]
Summary
Neuromyelitis optica (NMO; Devic’s disease) is a demyelinating inflammatory autoimmune disease of the central nervous system leading to recurrent optic neuritis (ON) and episodic myelitis [1,2,3]. In contrast to MS, disease attacks in patients with NMO are usually more severe and recover only partially. Apart from the deterioration of visual and motor function, the presence of severe pain in a substantial proportion of NMO patients with a high impact on their health-related quality of life was only recently reported [10,11]. The scale reflecting impairment of patients with multiple sclerosis (Expanded Disability Systems Score EDSS), which is frequently used to characterize dysfunction in patients with NMO, does not include any measure reflecting pain or hyperalgesia [12]. The presence of pain and the attending reduction in quality of life have been frequently overlooked and are underrepresented in most studies
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