Pain
-
We assessed pain characteristics and sensory profiles of a large and extensively phenotyped cohort of patients with polyneuropathies (PNPs) and small fiber neuropathy (SFN) using quantitative sensory testing (QST). Our aim was to detect potentially discriminative QST profiles of patient subgroups determined by pain, etiology, or skin innervation. We prospectively recruited 350 patients with painful and painless PNPs and with SFN at 1 neuromuscular center. ⋯ In healthy controls, skin innervation positively correlated with sensory thresholds, whereas this correlation was lost in patients with PNP and SFN. Quantitative sensory testing did not distinguish between painful and painless neuropathies regarding small fiber function, but revealed higher mechanical pain (P < 0.01) and detection thresholds (P < 0.05) and lower mechanical pain sensitivity in the group of patients with painful neuropathies. Etiological neuropathy subgroups were not distinguished by QST.
-
Communication within the brain is dynamic. Chronic pain can also be dynamic, with varying intensities experienced over time. Little is known of how brain dynamics are disrupted in chronic pain, or relates to patients' pain assessed at various timescales (eg, short-term state vs long-term trait). ⋯ Furthermore, greater dynamic connectivity with executive control networks was associated with milder NP, but greater dynamic connectivity with limbic networks was associated with greater NP. Compared with healthy individuals, the dFC features most highly related to trait NP were also more abnormal in patients with greater pain. Our findings indicate that dFC reflects patients' overall pain condition (ie, trait pain), not just their current state, and is impacted by complexities in pain features beyond intensity.
-
Sensory disturbances often spread beyond the site of injury in complex regional pain syndrome (CRPS) but whether this applies equally to CRPS I and II, or changes across the course of the disease, is unknown. Establishing this is important, because different symptom profiles in CRPS I and II, or in acute vs chronic CRPS, might infer different pathophysiology and treatment approaches. To explore these questions, sensory disturbances were assessed in the limbs and forehead of 71 patients with CRPS I and 33 patients with CRPS II. ⋯ Some of these hemisensory disturbances strengthened with chronicity of pain. These findings suggest that heightened excitability of nociceptive pathways in CRPS spreads to hemisensory convergence points in the brainstem or higher brain centres, possibly in association with compromised pain controls. The similarity of symptom profiles in chronic CRPS I and II implies shared mechanisms despite different triggers.