Fibromyalgia is characterized by what primary abnormality?

Fibromyalgia is characterized by what primary abnormality?

• A. Autoimmune attack on peripheral nerves
• B. Abnormal CNS pain transmission and processing
• C. Increased chest wall rigidity
• D. Overproduction of cortisol

Answer: (B)

Fibromyalgia revolves around abnormal pain processing in the central nervous system, meaning the brain and spinal cord amplify and interpret pain signals differently than in healthy individuals. This heightened sensitivity—often called central sensitization—makes ordinary stimuli feel painful and sustains a widespread sense of ache even when there isn’t clear tissue damage. Neurochemical changes in the CNS, such as lower levels of pain-inhibiting neurotransmitters like serotonin and norepinephrine and higher levels of substances that promote pain signaling, contribute to this exaggerated pain perception. Because the primary issue is how pain is processed and perceived by the CNS, fibromyalgia is not driven by an autoimmune attack on peripheral nerves, not by increased chest wall rigidity, and not by excess cortisol. Understanding this helps explain the broad, non-inflammatory pain pattern and guides treatments toward improving CNS pain modulation, sleep, and function rather than targeting immune processes or hormonal excess.

Fibromyalgia revolves around abnormal pain processing in the central nervous system, meaning the brain and spinal cord amplify and interpret pain signals differently than in healthy individuals. This heightened sensitivity—often called central sensitization—makes ordinary stimuli feel painful and sustains a widespread sense of ache even when there isn’t clear tissue damage. Neurochemical changes in the CNS, such as lower levels of pain-inhibiting neurotransmitters like serotonin and norepinephrine and higher levels of substances that promote pain signaling, contribute to this exaggerated pain perception. Because the primary issue is how pain is processed and perceived by the CNS, fibromyalgia is not driven by an autoimmune attack on peripheral nerves, not by increased chest wall rigidity, and not by excess cortisol. Understanding this helps explain the broad, non-inflammatory pain pattern and guides treatments toward improving CNS pain modulation, sleep, and function rather than targeting immune processes or hormonal excess.