Beta Electroencephalographic Oscillation Is a Potential GABAergic Biomarker of Chronic Peripheral Neuropathic Pain

Abstract

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.

EEG Beta functional connectivity decrease in the left amygdala correlates with the affective pain in fibromyalgia: A pilot study

“…Patients were recruited mainly through neurologists, rheumatologists and pain specialists from Fribourg Hospital, and through Swiss FM associations using web-based and flyer advertisements, while advertisements for controls targeted middle-aged adult hobby associations. Participants (cases and controls) were adult (≥18 y) females [ 1 ] and right-handed [ 9 ]. The diagnosis of FM had to be made by the specialists and meet internationally admitted criteria (see below).…”

“…The diagnosis of FM had to be made by the specialists and meet internationally admitted criteria (see below). Exclusion criteria consisted in: existence of central nervous system lesion or disease (including epilepsy and parasomnia), significant cognitive impairment, coexistence of any other type of pain (patients) or any pain (controls), and surgery involving any nervous system structure less than six months before inclusion [ 9 ].…”

“…Accordingly, substantial decrease in brain GABAergic signaling is reported in chronic pain patients [ 7 ], brain inhibition being mainly driven by GABAergic interneurons [ 8 ]. Furthermore, we recently showed reduction in EEG markers of the GABAergic neurotransmission, namely beta (β) oscillations, in chronic neuropathic pain [ 9 ]. Thus, we further assumed that expected power and FC changes in FM would be measurable through decrease in the EEG β oscillatory band.…”

The Affective Dimension of Pain Appears to Be Determinant within a Pain–Insomnia–Anxiety Pathological Loop in Fibromyalgia: A Case-Control Study

“…The diagnosis of FM had to be made by a specialist (rheumatologist, neurologist, or pain specialist) and meet internationally admitted diagnosis criteria (see below). All participants were adults (age ≥ 18 years old) and right-handed, following indications for possible lateralization in brain function related to chronic pain [ 35 ], including in FM [ 36 ]. In order to avoid data variability due to sex influence on pain perception [ 37 , 38 ] and taking into account the epidemiology of FM [ 39 ], we included exclusively females.…”

“…We assessed specific descriptors and correlations, except when analyzing the current (ongoing) pain intensity, knowing its emerging role in FM-related pathological modifications occurring in pain matrix [ 48 ]. Taking into account that the definition of successful analgesia is VAS < 3 [ 49 ] and that our previous data showed significant differences in pain-related neurophysiological EEG markers when VAS ≥ 3 [ 35 ], we considered the latter threshold to define a significant pain, even if other classifications of pain severity exist [ 43 , 50 ]. Additionally, pain was considered to be moderate and severe when VAS equaled, respectively, 4.5–7.4 and 7.5–10 [ 51 ].…”