Case report A 30-year-old woman, suffering from migraine without aura, employee, single, non-smoker, social drinker and regular sleep/wake routine. Comorbidity: ovarian endometriosis surgically treated. The patient reported headaches since the age of 14 at menarche and with episodic attacks (1-2 per month).
Two years ago the patient started an estroprogestinic (etinilestradiolo plus drospirenone) therapy and the headache worsened: the intensity of pain and frequency of attacks increased (about 8 per month) and also the analgesic consumption (about 10 SAID tablets per month).
The pain was throbbing, moderate to severe intensity and unilateral in frontal, temporal and orbital regions and it was associated with autonomic symptoms (photophobia, phonophobia, nausea and sometimes vomit). We suggested changing the type of estroprogestinic drug and prophylactic therapy with amytriptiline (16 mg/day). There were no benefits after three months of the suggested therapy: headache was unchanged and the patient gained weight (5 kg).
In the meanwhile, the gynecologist prescribed a drug to better control pelvic pain: palmitoylethanolamide (PEA), 3 tablets/day for three months.
After three months, the patient returned for a planned control visit and reported great improvement in headache frequency (4-5 attacks per month) and reduction in analgesic drug consumption and pelvic pain.
PEA is an endogenous fatty acid amide analogue of the endocannabinoid anandamide, it is synthesised during inflammation and tissue damage and has been shown to have a number of beneficial effects and to be useful in the control of neurogenic and neuropathic pain. The exact pathophysiogenetic mechanism of migraine and chronic pelvic pain are still unknown, but the role of mast cells is very important in both diseases .
Although its pharmacological efficacy is well known, the mechanism of action of this family of compounds is still unclear. It has been hypothesized that PEA could bind CB2 receptors on mast cells and sensory neurons, according to the ALIA mechanism of PEA (ALIA: Autacoid Local Injury Antagonism) and putative activation of cannabinoids and vanilloid TRPV1 receptors via “entourage” effects.