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Midodrine, also known as 3,6-dimethoxy-β-hydroxy-N-aminoethanonyl-2-phenylethylamine, is a substituted phenethylamine derivative. [4] Midodrine is an odorless, white, crystalline powder, soluble in water and sparingly soluble in methanol. [19] Midodrine's experimental log P is -0.5 and its predicted log P ranges from -0.49 to -0.95.
A systematic review and meta-analysis conducted on clinical trials comparing the clinical use of droxidopa and midodrine have found that midodrine was more likely to cause supine hypertension than droxidopa in patients with NOH. Midodrine was also found to be slightly more effective at raising blood pressure but not statistically significantly ...
The biology of depression is the attempt to identify a biochemical origin of depression, as opposed to theories that emphasize psychological or situational causes. Scientific studies have found that different brain areas show altered activity in humans with major depressive disorder (MDD) . [ 1 ]
Physical causes are ruled out with a clinical assessment of depression that measures vitamins, minerals, electrolytes, and hormones. [ 2 ] [ 3 ] [ 4 ] Though psychiatric medication is the most frequently prescribed therapy for major depression, [ 5 ] psychotherapy may be effective, either alone or in combination with medication. [ 6 ]
The neurotrophic hypothesis of depression [1] proposes that major depressive disorder (MDD) is caused, at least partly, by impaired neurotrophic support.Neurotrophic factors (also known as neurotrophins) are a family of closely related proteins which regulate the survival, development, and function of neurons in both the central and peripheral nervous systems.
It may cause depressed patients to be noncompliant in their treatment, and the effects of certain substances can worsen the effects of depression. Other psychiatric disorders that may predict treatment-resistant depression include attention deficit hyperactivity disorder , [ 7 ] personality disorders , obsessive compulsive disorder , and eating ...
The half-life of venlafaxine is about 5 hours, and with once-daily dosing, steady-state concentration is achieved after about 3 days, though its active metabolite desvenlafaxine lasts longer. [59] The half-life of desvenlafaxine is about 11 hours, and steady-state concentrations are achieved after 4 to 5 days. [ 58 ]
This is seen in that immune activity does not appear to be enough on its own to cause depression. [39] Evidence for this comes primarily from treatments that involve the pro-inflammatory IFN-α, which is commonly used in treating viral infections but only results in major depression in about one third of patients.