There is also a lot of cross-talk between the brain and immune system. For example, people sleeping much longer when they are sick is probably mediated by COX2 -> prostaglandins -> effects on the pre-optic area of the hypothalamus, which regulates sleep and I might also add houses oxytocinergic cells. As an aside, you may be interested in this ascorbic acid/pre-optic area study
https://www.ncbi.nlm.nih.gov/pubmed/24064109
Anyways,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3748818/
"There are two forms of COX: COX1 is constitutively active in many tissues, and COX2 is mainly induced during inflammatory responses
8. Although COX2 is expressed constitutively by some neurons in the brain, systemic LPS (*an inflammatory molecule) induces COX2 in the brain only in perivascular and endothelial cells along small venules, and IL-1β primarily activates COX2 in perivascular cells
9–11. These venules are found throughout the brain, but are densest in the
preoptic area"
The issues seen with some GABA interneurons in the hippocampus of animals given MDMA have been found to be mediated by COX-2/prostaglandins. Unfortunately they only studied the hippocampus.
At any rate, there is surely a neurological explanation as to why sickness -> anti-inflammatory medications -> resolution of sickness could have had an effect on Scratcher's symptoms. The cells that are acting via 5-HT2 receptor mediated induction of COX-2 and hence prostaglandin synthesis -> glutamate release to affect GABA interneurons in the hippocampus are astrocytes, which are no longer thought to be solely part of the "housekeeping/immune system" portion of the CNS - they are thought to play an integral role to the function of the brain.