anircCob sahdaeyrn btnhrioiis (,ge oza)almaedctie adn lopo diiucsrte e(,g uree)fsodmi rea toguhht ot treex ehtir eefctf on PIC by rdiencgu lbcaeprnoersi fidlu CS(F) dorunocipt ta the codrhoi selu.xp
Ggloeo sasy mmesinach is nwonunk LOL.
Tish iostnueq kmesa no enses to em. eSh sah na eyxtremle owl ginonep psrsruee tey sha ngsis of edcaneisr tilrnniaaarc r.eupsrse Ddi ethy naem ot tup 23 mc ?0?2??????H?
pSMeaced: midaetzolAaec" )(CZA dna oremsefudi U)RF( rteta stahrhporgiocme uhhdcyoarsple ni onenstae. othB era rduictesi thta losa aeappr ot ceeeadrs nroeicste fo FSC ta teh lleve fo teh rdicooh sep"lu.x
3-CHO is needde to mkea .CSF zdlmtaAeoeiac ihnibist icnrboca densahary nad eesarecd CO-H3 pabrntoosi rfmo laner tslubue.
In patients with IIH treated with acetazolamide, the inhibition of carbonic anhydrase in the choroid plexus results in a reduction of CSF production and flow. The acid–base status of the patient may also alter the distribution of acetazolamide in the CSF and brain, but its effect on the CSF flow is secondary to that mediated by the choroid plexus. Based on the pharmacology and distribution of acetazolamide and carbonic anhydrase in the brain, the theory that emphasizes the effect of acetazolamide on CSF production in IIH is most likely primary and direct, and weight loss, when recognized as a factor, is secondary and indirect, and frequently the result of toxic doses in excess of the amount needed for complete enzyme inhibition.