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There have been reports that quetiapine helps some of us with symptoms. It is my belief that part of the etiology of hppd, for those who are mast cell sensitive patients to begin with (upwards of 18% of population falls somewhere on this scale) benefit from quetiapine due to the antihistamine action on neuronal h1 receptors. For those of you that are unfamiliar, there is already a hypothesis on this website that the user Fawkinchit has written about concerning microglia and astrocyte activity releasing too much glutamate. Here I propose that for a subset of people with hppd, they also have mast cell activation— either through the direct action of the drug or through stress. The neuronal action is thus

Histamine is NOT just for allergies. There are many histamine receptors and they do many different things in modulating immune response to giving erections.

pns histamine, while unable to cross the blood brain barrier, does increase neuronal histamine levels. This article disputed that, however according to Dr Afrin, the most world rebound mast cell expert, there is a cascade that does in fact activate neuronal mast cells  even though histamine does not cross the BBB .


mast cell activation —> 2000 mediators release —> histamine is a major one; excitatory neurotransmitter—> activates microglia/ astrocyte—> induced rapid and uncontrolled/persistent glutamate release —> neuronal injury to glia/astrocyte and surrounding neurons —> the persistence of this mechanism does not allow the brain to heal.

this is where quetiapine can be helpful for some: 

“Quetiapine is a tricyclic H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.”


lamictal is another good choice for this same action 

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