The goal of this study is to test whether voluntary regulation of limbic system activation is possible in patients with fibromyalgia and to examine the neurobehavioral effects of specific neuromodulation of this circuit on somatosensory, limbic, and cognitive processes. This goal will be achieved by using a method previously developed for the construction of an fMRI-enriched EEG model ("EEG-Finger-Print", EFP) that selectively targets the amygdala BOLD activation (Amyg-EFP). The investigators conducted two studies: In the first study, the investigators conducted simultaneous recordings of EEG and fMRI during Amyg-EFP NF training on patients with FM. The main objective is to demonstrate target engagement following Amyg-EFP-NF training in FM patients. In the second study, the investigators aim to conduct a randomized clinical trial to examine the causal effect of the Amyg-EFP NF trial. The investigators will compare neurobehavioral effects between three groups. I. Amyg-EFP-NF group: a multisession NF trial using the Amyg-EFP model. II. Control group 1- sham-NF: a multisession NF trial using sham feedback. III. Control group 2: patients in this group will continue their usual treatment without intervention.
The current study aims to focus on the neural mechanism and brain-guided therapy of Fibromyalgia (FM); a chronic pain syndrome. Despite intense investigations, the pathophysiology of fibromyalgia remains elusive. Several studies demonstrated that morphological and functional changes in the central nervous system may play an important role in FM development and progression. The unknown etiopathology of FM contributed greatly to the absence of mechanism-specific cures. The insufficient treatment for FM, along with the understanding that CNS abnormality constitutes a major factor in FM pathophysiology, emphasizes the need for mechanism-based therapeutic intervention and opens the door for advanced neuromodulation techniques. Guided by this approach, the investigators aspired to establish a multi-function model with the potential to exert neuromodulation effects. To address this goal, the investigators employ a method previously developed for the construction of an fMRI-enriched EEG model ("EEG-Finger-Print", EFP). In this approach, EEG is used to predict specific brain activity, as measured by fMRI in a given region. Our main objective is to explore the neural mechanisms that underlie limbic neuromodulation and to gain a profound understanding of the functional processes that can potentially modify deficient functions in FM. The investigators intend to conduct two studies. In the first study, the investigators focus on the previously developed EFP model that selectively targets the amygdala BOLD activation (Amyg-EFP). The investigators aspired to investigate Amyg-EFP-NF effects on chronic pain in FM. To do so, the investigators conducted simultaneous recordings of EEG and fMRI during Amyg-EFP NF training on patients with FM. The main research objective of this study is to demonstrate target engagement following Amyg-EFP-NF training in FM patients. In the second study, the investigators aim to conduct a randomized clinical trial to examine the causal effect of the Amyg-EFP on patients with FM and to explore the clinical effect of this model on a wide range of symptoms related to FM. To examine the neural, clinical, and behavioral specific effects of the EFP-NF training, the investigators will implement a comprehensive clinical assessment. Furthermore, the investigators will conduct an MRI/fMRI scan before and after the EFP-NF trial, in order to explore the neural modification effects. Clinical follow-up will be conducted after 10-12 months from the post-intervention evaluation. The investigators will compare the neural, clinical, and behavioral effects between three groups. I. Amyg-EFP-NF group: a multisession NF trial using feedback driven by the Amyg-EFP model. II. Control group I- sham-NF: a multisession NF trial using sham feedback. III. Control group II: patients in this group will continue their usual treatment without any intervention. The investigators hypothesize that patients in the Amyg -EFP-NF group will exhibit wider and more robust changes in neural and behavioral outcomes associated with the wide range of symptoms related to FM. This study can significantly advance the understanding of the neural processes that mediate modification of somatic-affective functions in patients with FM and, therefore, enable the establishment of better treatment prediction and possibly more personalized procedures in future studies.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
TRIPLE
Enrollment
70
Neurofeedback training utilizing Amygdala Electrical Fingerprint (Amyg-EFP) methodology
Sham neurofeedback training based on a randomized artificial Amyg-EFP signal.
Tel Aviv Sourasky Medical Center
Tel Aviv, N/A = Not Applicable, Israel
Clinical improvement using the Fibromyalgia Impact Questionnaire (FIQ) to evaluate FM symptoms
Scoring from 0 (no impairment) to 80 (maximum), with subscales ranging up to 10 (maximum).
Time frame: Immediately post-intervention relative to the baseline level
Clinical improvement using the Symptom Severity Score (SSS)
Ranges from 0 to 12 (highest severity).
Time frame: Immediately post-intervention relative to the baseline level
Clinical improvement using the Widespread Pain Index (WPI)
Ranges from 0 to 19 (highest level of pain distribution).
Time frame: Immediately post-intervention relative to the baseline level
Clinical improvement using the SF-36 Health Survey (SF-36) to evaluate daily impacts of FM
Scores from 0 to 100 (higher scores indicate better health).
Time frame: Immediately post-intervention relative to the baseline level
Clinical improvement using the Trait Anxiety Inventory (STAI-T) to evaluate the level of anxiety
Ranges from 20 to 80 (highest anxiety level).
Time frame: Immediately post-intervention relative to the baseline level
Clinical improvement using the Beck Depression Inventory (BDI) to evaluate the level of depression
Ranges from 0 to 63 (highest depression level).
Time frame: Immediately post-intervention relative to the baseline level
Long-term clinical improvement using the Fibromyalgia Impact Questionnaire (FIQ) to evaluate FM symptoms
Scoring from 0 (no impairment) to 80 (maximum), with subscales ranging up to 10 (maximum).
Time frame: Change in symptoms at 10-12 months relative to the baseline level (Follow-up measure vs. Baseline)
Long-term clinical improvement using the Symptom Severity Score (SSS)
Ranges from 0 to 12 (highest severity).
Time frame: Change in symptoms at 10-12 months relative to the baseline level (Follow-up measure vs. Baseline)
Long-term clinical improvement using the Widespread Pain Index (WPI)
Ranges from 0 to 19 (highest level of pain distribution).
Time frame: Change in symptoms at 10-12 months relative to the baseline level (Follow-up measure vs. Baseline)
Long-term clinical improvement using the SF-36 Health Survey (SF-36) to evaluate daily impacts of FM
Scores from 0 to 100 (higher scores indicate better health).
Time frame: Change in symptoms at 10-12 months relative to the baseline level (Follow-up measure vs. Baseline)
Long-term clinical improvement using the Trait Anxiety Inventory (STAI-T) to evaluate the level of anxiety
Ranges from 20 to 80 (highest anxiety level).
Time frame: Change in symptoms at 10-12 months relative to the baseline level (Follow-up measure vs. Baseline)
Long-term clinical improvement using the Beck Depression Inventory (BDI) to evaluate the level of depression
Ranges from 0 to 63 (highest depression level).
Time frame: Change in symptoms at 10-12 months relative to the baseline level (Follow-up measure vs. Baseline)
Neural Prediction
Simultaneous fMRI/EEG scan in order to identify whether the Amyg-EFP signal reliably predicts the amygdala BOLD activity
Time frame: Through study completion, an average of 2 year
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