Fibromyalgia is a condition where patients experience chronic generalised pain, fatigue, tiredness, muscle stiffness, mood disturbances, waking up not well rested and memory problems. The muscles of patients with fibromyalgia have no pathology, therefore making this condition a pain disorder.
The diagnosis of fibromyalgia is made by identifying the following criteria:
- There must be chronic widespread pain on both sides of the body and above and below the waist.
- There must be tenderness experienced when pressure is applied to at least 11 out of 18 specific points on the body.
Fibromyalgia and thyroid disease
When these criteria were studied, it was determined thatnearly half of patients with autoimmune thyroid conditions, such as Hashimoto’s disease, also have symptoms of fibromyalgia. Conversely, it was noted that nearly 20% of patients with fibromyalgia have autoimmune thyroid conditions. Therefore, a strong correlation between these two conditions is present.
It’s noted that the symptoms of Hashimoto’s diseaseare similar to those of fibromyalgia. It’s therefore not so easy to distinguish whether symptoms are resulting from the thyroiditis or from fibromyalgia.
In order to help distinguish between the two conditions, patients diagnosed with fibromyalgia should be tested for hypothyroidism and patients with autoimmune thyroid disease, who experience pain syndromes, must be properly assessed to determine whether their pain symptoms suggest fibromyalgia.
Pain experienced in thyroid disease
The following are factors that are involved in pain being experienced in thyroid diseases.
- TSH – mediated: Increased levels of thyroid stimulating hormone (TSH) in untreated hypothyroidism results in pain and stiffness. This statement is strengthened by the fact that correcting thyroid hormone imbalances results in improvement of muscle pain in most patients. Not all patients respond to this treatment though, and this indicates that other mechanisms also play a part.
- Central sensitization: The glial cells in the brain secrete molecules that enhance sensitivity to pain in the central nervous system, and this is called central sensitization. These glial cells are affected by thyroid hormones and a thyroid imbalance will then negatively affect the functioning of these cells. When the functioning of these cells is disturbed then generalized pain, such as in fibromyalgia, is experienced.
- Small fibre polyneuropathy: Patients with Hashimoto’s disease experience a condition called small fibre polyneuropathy. This condition is defined as dysfunction or damage of small peripheral nerve fibres and this elicits symptoms such as pins and needles, burning pains and shooting pains.
- Inflammation: Molecules released in inflammatory conditions, such as cytokines, play a major role in generating chronic pain. Since there is a strong inflammatory component associated with Hashimoto’s disease, it can be said that cytokines would contribute to chronic pain in these patients.
- Immunologic cross reactivity: Anti-thyroglobulin antibodies, produced in Hashimoto’s disease, could act against acetyl cholinesterase leading to altered pain signalling by the central nervous system. This occurs since thyroglobulin and acetyl cholinesterase share structural similarities.
Central sensitization and small fibre neuropathy most probably results in fibromyalgia in patients diagnosed with Hashimoto’sdisease. These patients are managed with neuro-active medications such as gabapentin or pregabalin. Treatment with anti-inflammatory or immune-modulating agents is effective in patients where a strong inflammatory or immunological component is present.