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- Corticomotor excitability is altered in central neuropathic pain compared with non-neuropathic pain or pain-free patients(2023) BARBOSA, Luciana Mendonca; VALERIO, Fernanda; SILVA, Valquiria Aparecida da; RODRIGUES, Antonia Lilian de Lima; GALHARDONI, Ricardo; YENG, Lin Tchia; JUNIR, Jefferson Rosi; CONFORTO, Adriana Bastos; LUCATO, Leandro Tavares; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi deObjectives: Central neuropathic pain (CNP) is associated with altered corticomotor excitability (CE), which can potentially provide insights into its mechanisms. The objective of this study is to describe the CE changes that are specifically related to CNP.Methods: We evaluated CNP associated with brain injury after stroke or spinal cord injury (SCI) due to neuromyelitis optica through a battery of CE measurements and comprehensive pain, neurological, functional, and quality of life assessments. CNP was compared to two groups of patients with the same disease: i. with non-neuropathic pain and ii. without chronic pain, matched by sex and lesion location.Results: We included 163 patients (stroke=93; SCI=70: 74 had CNP, 43 had non-neuropathic pain, and 46 were pain-free). Stroke patients with CNP had lower motor evoked potential (MEP) in both affected and unaffected hemispheres compared to non-neuropathic pain and no-pain patients. Patients with CNP had lower amplitudes of MEPs (366 mu V +/- 464 mu V) than non-neuro-pathic (478 +/- 489) and no-pain (765 mu V +/- 880 mu V) patients, p < 0.001. Short-interval intracorti-cal inhibition (SICI) was defective (less inhibited) in patients with CNP (2.6 +/- 11.6) compared to no-pain (0.80.7), p = 0.021. MEPs negatively correlated with mechanical and cold-induced allo-dynia. Furthermore, classifying patients' results according to normative data revealed that at least 75% of patients had abnormalities in some CE parameters and confirmed MEP findings based on group analyses.Discussion: CNP is associated with decreased MEPs and SICI compared to non-neuropathic pain and no-pain patients. Corticomotor excitability changes may be helpful as neurophysiological markers of the development and persistence of pain after CNS injury, as they are likely to pro-vide insights into global CE plasticity changes occurring after CNS lesions associated with CNP.(c) 2023 The Author(s).
- Mirror peripheral neuropathy and unilateral chronic neuropathic pain: insights from asymmetric neurological patterns in leprosy(2023) RAICHER, Irina; ZANDONAI, Alexandra P.; ANGHINAH, Isadora W.; FRASSETTO, Mariana; STUMP, Patrick R. N. A. G.; TRINDADE, Maria A. B.; HARNIK, Simone; OLIVEIRA, Rodrigo A.; MACARENCO, Ricardo S. S.; DOPPLER, Kathrin; UCEYLER, Nurcan; MELLO, Evandro S.; SOMMER, Claudia; TEIXEIRA, Manoel J.; GALHARDONI, Ricardo; ANDRADE, Daniel C. deLeprosy-related multiple mononeuropathy offers a pattern of impairment where neuropathy with and without neuropathic pain (NeP) are present in the same individual, thus allowing to investigate peripheral sensory and innervation in both conditions. This cross-sectional study collected data on clinical and neurological examination, pain assessment questionnaires, quantitative sensory test, and intraepidermal nerve fiber density of patients with leprosy and divided the cohort into 2 groups: with NeP (P+) and without NeP (P-). Furthermore, we assessed mirror body areas in the same NeP individuals with bilateral neuropathy also presenting unilateral NeP. Pain-free patients having unilateral neuropathy were controls. A total of 37 P+ and 22 P- patients were evaluated. Limb areas with NeP had signs of C-fiber dysfunction and hyperesthesia on quantitative sensory testing compared with limb areas having neuropathy without NeP. Skin denervation was found in all patients with leprosy. Comparisons of limbs with and without neuropathy and with and without NeP revealed that higher heat pain thresholds (HPTs) were associated with neuropathic pain areas, whereas less altered HPT was correlated with higher fiber density. Furthermore, a relationship was found between time of leprosy treatment termination and more intense neuropathy, expressed by HPT increasing 0.03 degrees C each month. As expected, interindividual comparisons failed to show differences in intraepidermal nerve fiber density and subepidermal plexus areas between P+ and P- patients (P = 0.2980, P = 0.9044; respectively). Higher HPT and lower mechanical detection threshold were related to NeP. This study pointed out the relevance of intraindividual comparisons including mirror areas when assessing local changes in peripheral NeP.
- Site matters: Central neuropathic pain characteristics and somatosensory findings after brain and spinal cord lesions(2023) BARBOSA, Luciana Mendonca; VALERIO, Fernanda da; PEREIRA, Samira Luisa Apostolos; SILVA, Valquiria Aparecida da; RODRIGUES, Antonia Lilian de Lima; GALHARDONI, Ricardo; YENG, Lin Tchia; JR, Jefferson Rosi; CONFORTO, Adriana Bastos; LUCATO, Leandro Tavares; LEMOS, Marcelo Delboni; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi deBackground: It is unknown if different etiologies or lesion topographies influence central neuropathic pain (CNP) clinical manifestation.Methods: We explored the symptom-somatosensory profile relationships in CNP patients with different types of lesions to the central nervous system to gain insight into CNP mechanisms. We compared the CNP profile through pain descriptors, standardized bedside examination, and quantitative sensory test in two different etiologies with segregated lesion locations: the brain, central poststroke pain (CPSP, n = 39), and the spinal cord central pain due to spinal cord injury (CPSCI, n = 40) in neuromyelitis optica.Results: Results are expressed as median (25th to 75th percentiles). CPSP presented higher evoked and paroxysmal pain scores compared to CPSCI (p < 0.001), and lower cold thermal limen (5.6? [0.0-12.9]) compared to CPSCI (20.0? [4.2-22.9]; p = 0.004). CPSCI also had higher mechanical pain thresholds (784.5 mN [255.0-1078.0]) compared to CPSP (235.2 mN [81.4-1078.0], p = 0.006) and higher mechanical detection threshold compared to control areas (2.7 [1.5-6.2] vs. 1.0 [1.0-3.3], p = 0.007). Evoked pain scores negatively correlated with mechanical pain thresholds (r = -0.38, p < 0.001) and wind-up ratio (r = -0.57, p < 0.001).Conclusions: CNP of different etiologies may present different pain descriptors and somatosensory profiles, which is likely due to injury site differences within the neuroaxis. This information may help better design phenotype mechanism correlations and impact trial designs for the main etiologies of CNP, namely stroke and spinal cord lesions. This study provides evidence that topography may influence pain symptoms and sensory profile. The findings suggest that CNP mechanisms might vary according to pain etiology or lesion topography, impacting future mechanism-based treatment choices.
- Parkinson's Disease-related Pains are Not Equal: Clinical, Somatosensory and Cortical Excitability Findings in Individuals With Nociceptive Pain(2023) BARBOZA, Victor Rossetto; KUBOTA, Gabriel Taricani; SILVA, Valquiria Aparecida da; BARBOSA, Luciana Mendonca; ARNAUT, Debora; RODRIGUES, Antonia Lilian de Lima; GALHARDONI, Ricardo; CURY, Rubens Gisbert; BARBOSA, Egberto Reis; BRUNONI, Andre Russowsky; TEIXEIRA, Manoel Jacobsen; ANDRADE, Daniel Ciampi deChronic pain is a frequent and burdensome nonmotor symptom of Parkinson's disease (PD). PD-related chronic pain can be classified as nociceptive, neuropathic, or nociplastic, the former being the most frequent subtype. However, differences in neurophysiologic profiles between these pain subtypes, and their potential prognostic and therapeutic implications have not been explored yet. This is a cross-sectional study on patients with PD (PwP)-related chronic pain (ie, started with or was aggravated by PD). Subjects were assessed for clinical and pain characteristics through ques-tionnaires and underwent quantitative sensory tests and motor corticospinal excitability (CE) eva-luations. Data were then compared between individuals with nociceptive and non-nociceptive (ie, neuropathic or nociplastic) pains. Thirty-five patients were included (51.4% male, 55.7 +/- 11.0 years old), 20 of which had nociceptive pain. Patients with nociceptive PD-related pain had lower warm detection threshold (WDT, 33.34 +/- 1.39 vs 34.34 +/- 1.72, P = .019) and mechanical detection threshold (MDT, 2.55 +/- 1.54 vs 3.86 +/- .97, P = .007) compared to those with non-nociceptive pains. They also presented a higher proportion of low rest motor threshold values than the non-nociceptive pain ones (64.7% vs 26.6%, P = .048). In non-nociceptive pain patients, there was a negative corre-lation between WDT and non-motor symptoms scores (r = -.612, P = .045) and a positive correlation between MDT and average pain intensity (r = .629, P = .038), along with neuropathic pain symptom scores (r = .604, P = .049). It is possible to conclude that PD-related chronic pain subtypes have dis-tinctive somatosensory and CE profiles. These preliminary data may help better frame previous contradictory findings in PwP and may have implications for future trial designs aiming at developing individually-tailored therapies. Perspective: This work showed that PwP-related nociceptive chronic pain may have distinctive somatosensory and CE profiles than those with non-nociceptive pain subtypes. These data may help shed light on previous contradictory findings in PwP and guide future trials aiming at developing individually-tailored management strategies. (c) 2023 The Author(s).