Isotretinoin and many SSRIs can cause a long-term decrease in libido and other sexual functions, even after users of those drugs have shown improvement in their depression and have stopped usage. Multiple studies have shown that with the exception of bupropion (Wellbutrin), trazodone (Desyrel) and nefazodone (Serzone), antidepressants generally will lead to lowered libido. SSRIs that typically lead to decreased libido are fluoxetine (Prozac), paroxetine (Paxil), fluvoxamine (Luvox), citalopram (Celexa) and sertraline (Zoloft). Some antidepressant users have tried decreasing their dosage in the hopes of maintaining an adequate sex drive. Other users try enrolling in psychotherapy to solve depression-related issues of libido. However, the effectiveness of this therapy is mixed, with many reporting that it had no or little effect on sexual drive.Testosterone is one of the hormones controlling libido in human beings. Emerging research is showing that hormonal contraception methods like oral contraceptive pills (which rely on estrogen and progesterone together) are causing low libido in females by elevating levels of sex hormone-binding globulin (SHBG). SHBG binds to sex hormones, including testosterone, rendering them unavailable. Research is showing that even after ending a hormonal contraceptive method, SHBG levels remain elevated and no reliable data exists to predict when this phenomenon will diminish.Oral contraceptives lower androgen levels in users, and lowered androgen levels generally lead to a decrease in sexual desire. However, usage of oral contraceptives has shown to typically not have a connection with lowered libido in women.
Middle cerebral artery syndrome is a condition whereby the blood supply from the middle cerebral artery (MCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the lateral aspects of frontal, temporal and parietal lobes, the corona radiata, globus pallidus, caudate and putamen. The MCA is the most common site for the occurrence of ischemic stroke.Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with MCA syndrome. More distal blockages tend to produce milder deficits due to more extensive branching of the artery and less ischemic response. In contrast, the most proximal occlusions result in widespread effects that can lead to significant cerebral edema, increased intracranial pressure, loss of consciousness and could even be fatal. In such occasions, mannitol (osmotic diuretic) or hypertonic saline are given to draw fluid out of the edematous cerebrum to minimise secondary injury. Hypertonic saline is better than mannitol, as mannitol being a diuretic will decrease the mean arterial pressure and since cerebral perfusion is mean arterial pressure minus intracranial pressure, mannitol will also cause a decrease in cerebral perfusion. Contralateral hemiparesis and hemisensory loss of the face, upper and lower extremities is the most common presentation of MCA syndrome. Lower extremity function is more spared than that of the faciobrachial region. The majority of the primary motor and somatosensory cortices are supplied by the MCA and the cortical homunculus can, therefore, be used to localize the defects more precisely.