This preliminary investigation aimed to assess beta (β) oscillation, a marker of the brain GABAergic signaling, as a potential objective pain marker, hence contributing at the same time to the mechanistic approach of pain management. This case–control observational study measured β electroencephalographic (EEG) oscillation in 12 right-handed adult male with chronic neuropathic pain and 10 matched controls (∼55 years). Participants were submitted to clinical evaluation (pain visual analog scale, Hospital Anxiety, and Depression scale) and a 24-min high-density EEG recording (BIOSEMI). Data were analyzed using the EEGlab toolbox (MATLAB), SPSS, and R. The global power spectrum computed within the low (Lβ, 13–20 Hz) and the high (Hβ, 20–30 Hz) β frequency sub-bands was significantly lower in patients than in controls, and accordingly, Lβ was negatively correlated to the pain visual analog scale (R = −0.931, p = 0.007), whereas Hβ correlation was at the edge of significance (R = −0.805; p = 0.053). Patients’ anxiety was correlated to pain intensity (R = 0.755; p = 0.003). Normalization of the low and high β global power spectrum (GPS) to the GPS of the full frequency range, while confirming the significant Lβ power decrease in chronic neuropathic pain patients, vanished the significance of the Hβ decrease, as well as the correlation between Lβ power and pain intensity. Our results suggest that the GABAergic Lβ EEG oscillation is affected by chronic neuropathic pain. Confirming the Lβ GPS decrease and the correlation with pain intensity in larger studies would open new opportunities for the clinical application of gamma-aminobutyric acid-modifying therapies.

Fibromyalgia (FM) is a major chronic pain disease with prominent affective disturbances, and pain-associated changes in neurotransmitters activity and in brain connectivity. However, correlates of affective pain dimension lack. The primary goal of this correlational cross-sectional case-control pilot study was to find electrophysiological correlates of the affective pain component in FM. We examined the resting-state EEG spectral power and imaginary coherence in the beta (β) band (supposedly indexing the GABAergic neurotransmission) in 16 female patients with FM and 11 age-adjusted female controls. FM patients displayed lower functional connectivity in the High β (Hβ, 20–30 Hz) sub-band than controls (p = 0.039) in the left basolateral complex of the amygdala (p = 0.039) within the left mesiotemporal area, in particular, in correlation with a higher affective pain component level (r = 0.50, p = 0.049). Patients showed higher Low β (Lβ, 13–20 Hz) relative power than controls in the left prefrontal cortex (p = 0.001), correlated with ongoing pain intensity (r = 0.54, p = 0.032). For the first time, GABA-related connectivity changes correlated with the affective pain component are shown in the amygdala, a region highly involved in the affective regulation of pain. The β power increase in the prefrontal cortex could be compensatory to pain-related GABAergic dysfunction.

Graves’ disease (GD) is an autoimmune pathology characterized by hyperthyroidism and the presence of specific anti-thyroid antibodies. Neurological symptoms such as seizures, cognitive impairment, and tremor can be observed during the course of GD, but more complex movement disorders such as chorea and myoclonus are less frequent. The mechanisms underlying movement disorders in GD are not fully understood. While some authors relate movement disorders to thyroid dysfunction, others claim an autoimmune origin. We herein report a case involving a 60-year-old woman who presented with erratic, intricate movement disorders for which a medical workup revealed GD. During the 2-year follow-up period, her neurological symptoms evolved in parallel with her thyroid function, but not with her autoimmune anti-thyroid antibody level. Her neurological symptoms completely disappeared when she became euthyroid. We herein discuss the complicated clinicobiological relationship between thyroid function and movement disorders. This relationship involves several factors, including the impact of radioactive treatment. The present case emphasizes the importance of including thyroid function screening in the workup of unexplained movement disorders.

This study aimed at evaluating the impact of seasons on the nutritional status and on dietary cassava-related cyanide exposure in Burhinyi and Idjwi, two areas in the eastern Democratic Republic of the Congo, witnessing similarly high cassava-derived cyanide poisoning but differently affected by konzo and malnutrition. Cyanide content in cassava roots and flour, and urinary thiocyanate levels (uSCN) of 54 subjects (40 from Burhinyi and 14 from Idjwi, aged 28.7 (12.1) years, 63% women) were measured during the rainy season (RS) and dry season (DS), using picrate paper kits A and D1. Local processing methods proved to be efficient in removing cyanogenic compounds in fresh cassava roots during the RS. However, the cyanide content in flour samples significantly increased during DS, with ~50% of samples containing unsafe levels (>10 ppm) of cyanide content. Strikingly, the uSCN (µmol/L), from being comparably high in RS (~172.0), slightly decreased during DS in Burhinyi (~103.2; p = 0,3547), but not in Idjwi (~172; p = 0,1113). Furthermore, serum proteins and albumin levels significantly decreased during the DS, witnessing a worsening of nutritional status, in Burhinyi but not in Idjwi. The consumption of bitter cassava roots (OR = 5.43, p = 0.0144) and skipping heap fermentation (OR = 16.67, p = 0.0021) were independently associated with very high uSCN levels during the DS. Thus, restoring the traditional processing methods, and complying with them in either season should ensure the safe consumption of cassava.

Background: Fibromyalgia (FM) is a chronic pain disease characterized by multiple symptoms whose interactions and implications in the disease pathology are still unclear. This study aimed at investigating how pain, sleep, and mood disorders influence each other in FM, while discriminating between the sensory and affective pain dimensions. Methods: Sixteen female FM patients were evaluated regarding their pain, while they underwent—along with 11 healthy sex- and age-adjusted controls—assessment of mood and sleep disorders. Analysis of variance and correlations were performed in order to assess group differences and investigate the interactions between pain, mood, and sleep descriptors. Results: FM patients reported the typical widespread pain, with similar sensory and affective inputs. Contrary to controls, they displayed moderate anxiety, depression, and insomnia. Affective pain (but neither the sensory pain nor pain intensity) was the only pain indicator that tendentially correlated with anxiety and insomnia, which were mutually associated. An affective pain–insomnia–anxiety loop was thus completed. High ongoing pain strengthened this vicious circle, to which it included depression and sensory pain. Conclusions: Discriminating between the sensory and affective pain components in FM patients disclosed a pathological loop, with a key role of affective pain; high ongoing pain acted as an amplifier of symptoms interaction. This unraveled the interplay between three of most cardinal FM symptoms; these results contribute to better understand FM determinants and pathology and could help in orienting therapeutic strategies.