Has anyone tried this third generation beta blocker? apparently its 10x better then propranolol.
Carvedilol also blocks alpha receptors, which are found on blood vessels, and relaxes the blood vessels, dilating them, which lowers blood pressure and vascular resistance.
By comparison, propranonol is an indirect α1 adrenoceptor agonist and has sodium channel blocking effects. Thus, while both drugs are potent β-adrenoceptor antagonists, carvedilol’s additional status as an α1 adrenoceptor antagonist would likely make it contraindicated for patients with erythromelalgia. Carvedilol would make erythromelalgia symptoms worse, not better.
Edit 1:
Propranonol = indirect α1 adrenoceptor agonist
Carvedilol = α1 adrenoceptor antagonist
That means where carvedilol is blocking α1 adrenoceptors, propranonol is indirectly activating α1 adrenoceptors. How this affects peripheral blood vessels is very important for patients with erythromelalgia.
Edit 2:
Studies have demonstrated propranolol’s ability to block cardiac, neuronal, and skeletal voltage-gated sodium channels, accounting for its known membrane stabilizing effect and antiarrhythmic and other central nervous system effects.
That is probably why propranonol is sometimes beneficial for erythromelalgia. My erythromelalgia is most responsive to the sodium channel blocker mexiletine, but I also find propranonol to be modestly beneficial.
Propranonol’s status as a beta blocker is probably not what is beneficial for erythromelalgia.
Hey Carter,
Check this article and tell me what you think? It states this affliction is a possible version of erythromelagia, and carvidilol got rid of it.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5597881/
And thanks for the information on the difference 
I think Prevost is wrong. Erythromelalgia simply doesn’t resolve in the manner described. It soon reoccurs if a successful pharmacological treatment is stopped. Narang’s hypothesis that red scrotum syndrome resembles rosacea is likely more accurate.
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