Impaired neurosteroid synthesis in multiple sclerosis

The attention impairments in MHE are observed on a variety of measures. These include measures of cognitive processing speed involving psychomotor responding, such as the Number Connection tests (NCT), block design test (BDT),the Digit Symbol test (DST), line drawing test, circle-dotting test, serial-dotting test, figure connection test. Impairments on measures of cognitive processing speed and response inhibition that do not require a motor response have also been reported (., with verbal fluency tasks and measures such Stroop test). 22,23 Visuospatial impairments have been primarily reported on block design tasks (which also include a motor/practic component), but also on more pure measures of visuospatial perception, such as line orientation or the Hooper test. Fine motor skill impairments have been noted on measures such as the grooved pegboard task, and on line tracing tasks (the latter also involve visuospatial abilities). 24

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The second isoenzyme of 5α reductase is deficient in the classic intersex condition ( pseudovaginal perineoscrotal hypospadias ), or 5α-reductase deficiency . It was first discovered in indigenous cultures of Papua, New Guinea , where children were born with feminine genitalia in the absence of endogenous DHT during pregnancy, but with the surge of testosterone during adolescence, changed to males at puberty. Because of this change at puberty, the condition is also sometimes called " guevedoche ." [24] There is a range of external appearance that has been described of external genitalia at birth, with varying degrees of virilization.

Unlike benzodiazepines, etifoxine appears to produce its anxiolytic effects by activating β2 and β3 subunit containing channels of the GABA A receptor complex (a different binding site than benzodiazepines), and by stimulating the production of GABA(A) active neurosteroids that act in conjunction with etifoxine's direct effects. [9] This difference in binding means that etifoxine can be used alongside benzodiazepines to potentiate their effects without competing for binding sites; [10] however, it also means that the effects of etifoxine are not reversed by the benzodiazepine antagonist flumazenil . [11]

Impaired neurosteroid synthesis in multiple sclerosis

impaired neurosteroid synthesis in multiple sclerosis

Unlike benzodiazepines, etifoxine appears to produce its anxiolytic effects by activating β2 and β3 subunit containing channels of the GABA A receptor complex (a different binding site than benzodiazepines), and by stimulating the production of GABA(A) active neurosteroids that act in conjunction with etifoxine's direct effects. [9] This difference in binding means that etifoxine can be used alongside benzodiazepines to potentiate their effects without competing for binding sites; [10] however, it also means that the effects of etifoxine are not reversed by the benzodiazepine antagonist flumazenil . [11]

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