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Researchers identified 3 subgroups of patients with peripheral neuropathic pain, based on sensory signs and symptoms. Their findings were published in Pain.1
Clinical trials currently classify and evaluate peripheral neuropathic pain based on etiology. This approach may not be adequate because of the heterogeneity of pain processes underlying these disorders, which may explain the low success rates of current treatments.1,2 In addition, individuals with neuropathic pain resulting from the same etiology may differ in their development of sensory signs and symptoms.3
However, certain sensory findings may be linked to a specific pain process, such as hyperalgesia with peripheral sensitization.4 Thus, patterns of sensory signs, or somatosensory profiles, may indicate dysfunction in afferent processing that may respond differently to treatment from 1 patient to another.
By performing a cluster analysis on patient data from the German Neuropathic Pain Research Network and the EUROPAIN and NEUROPAIN consortia, researchers classified patients with peripheral neuropathic pain into subgroups with distinct characteristics.
A total of 902 patients were included in the test cohort, and 233 patients were in the validation cohort. Etiologies of neuropathic pain included postherpetic neuralgia, polyneuropathy, radiculopathy, and peripheral nerve injury.
A total of 3 different somatosensory profiles were identified: sensory loss, exhibiting sensory deficits such as loss of pinprick sensitivity; thermal hyperalgesia, with increased thermal pain sensitivity; and mechanical hyperalgesia, characterized by allodynia in response to mechanical stimulus such as pinprick. The prevalence rates of these profiles in the study population were 42%, 33%, and 24%, respectively.
All 3 profiles were represented in each etiology evaluated, although there were differences in their distribution. Sensory loss was the most common profile for polyneuropathy and radiculopathy, whereas thermal hyperalgesia was the least common for patients with diabetic polyneuropathy.
The researchers noted that the profiles identified in this study correspond to the characteristics of populations in several clinical trials, suggesting the efficacy of some therapies may differ between somatosensory profiles.
Summary and Clinical Applicability
The limited success of current treatments for peripheral neuropathic pain suggests that better systems for classifying patients in clinical trials are needed. Researchers identified 3 somatosensory profiles, or subgroups, that may correlate with pain processes and may predict response to treatment.
“We present a new approach of subgrouping patients with peripheral neuropathic pain of different etiologies according to intrinsic sensory profiles. These 3 profiles may be related to pathophysiological mechanisms and may be useful in clinical trial design to enrich the study population for treatment responders,” the researchers wrote.
Limitations and Disclosures
Each research network had different inclusion criteria, so the populations for each etiology for neuropathic pain were not homogeneous.
The data analysis evaluated only the short-term stability of the somatosensory profiles; it is possible that patients may exhibit different somatosensory profiles over time.
The researchers report financial relationships with multiple pharmaceutical companies.
References
- Baron R, Maier C, Attal N, et al. Peripheral neuropathic pain: a mechanism-related organizing principle based on sensory profiles. Pain. 2017;158(2):261-272. doi: 10.1097/j.pain.0000000000000753
- Finnerup NB, Attal N, Haroutounian S, et al. Pharmacotherapy for neuropathic pain in adults: a systematic review and meta-analysis. Lancet Neurol. 2015;14(2):162-173. doi: 10.1016/S1474-4422(14)70251-0
- Maier C, Baron R, Tölle TR, et al. Quantitative sensory testing in the German Research Network on Neuropathic Pain (DFNS): somatosensory abnormalities in 1236 patients with different neuropathic pain syndromes. Pain. 2010;150(3):439-450. doi: 10.1016/j.pain.2010.05.002
- LaMotte RH, Thalhammer JG, Torebjörk HE, Robinson CJ. Peripheral neural mechanisms of cutaneous hyperalgesia following mild injury by heat. J Neurosci. 1982;2(6):765-781.
