Fibromyalgia is a chronic condition causing widespread pain, fatigue, sleep disturbances, and cognitive difficulties. It affects millions, with a higher prevalence in women. While its cause is not singular, research suggests symptoms stem from complex changes within the brain and central nervous system.
Physical and Activity Differences in the Brain
Advanced imaging techniques, such as MRI, reveal structural and functional differences in the brains of individuals with fibromyalgia. Reduced gray matter volume is a notable finding in several pain-processing regions. Areas like the anterior cingulate cortex, prefrontal cortex, and insula, involved in sensory and emotional pain processing, often show this reduction. These gray matter changes, in tissue containing neuronal cell bodies, may explain altered pain perception.
Changes also appear in white matter, the brain’s communication pathways. Deviations suggest altered conduction of pain signals, with altered transmission observed in the thalamus, a key pain processing hub. These structural alterations correlate with a patient’s reported pain perception.
Functional brain activity patterns also differ. Studies show altered connectivity within and between brain networks, including the default mode network (DMN) and salience network (SN). The DMN, active during rest and self-referential thinking, can show decreased connectivity, while the SN, involved in processing sensory input, may exhibit increased connectivity, particularly between the insula and anterior cingulate cortex. These altered connectivity patterns contribute to the diverse symptoms experienced by those with the condition.
How Pain is Processed Differently
Central sensitization is a core concept in fibromyalgia pain, where the central nervous system becomes hypersensitive to pain signals. This means mild stimuli can be amplified, leading to heightened pain perception (hyperalgesia), or even pain from non-painful stimuli (allodynia). The brain’s pain matrix, including regions like the thalamus, somatosensory cortex, anterior cingulate cortex, and insula, processes pain differently. These areas may show increased neural activity in response to painful stimuli.
The brain’s ability to regulate pain through descending inhibitory pathways also appears dysfunctional. These pathways normally modulate incoming pain signals. In fibromyalgia, reduced activity in pain-inhibiting systems or increased activity in pain-facilitating pathways creates an an imbalance. This makes the brain less effective at dampening pain signals, allowing them to be amplified throughout the body.
Reduced descending inhibition leads to widespread deep pain, tenderness, and increased responses to noxious stimuli. Lower levels of certain neurotransmitter metabolites in the cerebrospinal fluid, involved in these pathways, support this dysfunction. Amplified pain processing and dysfunctional pain modulation contribute to the chronic, widespread pain characteristic of fibromyalgia.
Understanding Fibro Fog
Fibro fog describes cognitive symptoms frequently experienced by individuals with fibromyalgia. These include difficulties with memory, attention, concentration, and information processing speed. Patients often report problems with immediate and delayed recall, and sustained auditory concentration, with subjective memory deficits sometimes exceeding objective ones. These cognitive impairments can be triggered by stress and worsened by pain.
Brain mechanisms underlying fibro fog include altered activity in regions associated with executive function and memory. The prefrontal cortex, involved in executive functions, and the hippocampus, which plays a significant role in learning and memory, are implicated. Studies show reduced hippocampal volume in fibromyalgia, which may contribute to memory complaints.
Excessive neurotransmitter consumption due to heightened pain sensitization may deplete neural resources needed for other brain functions, including cognition. Altered brain connectivity also impacts cognitive performance. Unlike a healthy brain, the fibromyalgia brain experiences disruptions that lead to these noticeable cognitive challenges.
Chemical and Inflammatory Changes
Neurochemical imbalances are a significant aspect of the fibromyalgia brain, affecting neurotransmitters involved in pain modulation, mood, and sleep. Serotonin, norepinephrine, and dopamine are key neurotransmitters implicated. Lowered serotonin and norepinephrine in the central nervous system may contribute to dysfunctional descending pain pathways and reduced pain inhibition. Low dopamine levels also contribute to pain and cognitive difficulties.
In contrast, excitatory neurotransmitters, such as glutamate and substance P, are often elevated in the cerebrospinal fluid and certain brain regions. Elevated glutamate levels in pain processing areas like the insula, amygdala, and cingulate cortex correlate with lower pressure pain thresholds. This imbalance between pain-enhancing and pain-inhibiting chemicals contributes to augmented pain processing.
Neuroinflammation is also present in fibromyalgia. Glial cells, the immune cells of the central nervous system (microglia and astrocytes), become activated. These activated glial cells release pro-inflammatory cytokines (e.g., IL-6, IL-8, TNF-α), which can sensitize pain pathways and contribute to widespread pain and fatigue. This neuroinflammatory process, alongside neurotransmitter imbalances, plays a role in the chronic symptoms experienced by those with fibromyalgia.