Browns syndrome is a rare form of strabismus characterized by limited elevation of the affected eye. The disorder may be congenital (existing at or before birth), or acquired. Brown syndrome is caused by a malfunction of the superior oblique muscle, causing the eye to have difficulty moving up, particularly during adduction (when eye turns towards the nose). Harold W. Brown first described the disorder in 1950 and initially named it the "superior oblique tendon sheath syndrome". Presentation
A simple definition of the syndrome is "limited elevation in adduction from mechanical causes around the superior oblique". This definition indicates that when the head is upright, the eye is restricted in movement due to problems with muscles and tendons that surround the eye.Harold W. Brown characterized the syndrome in many ways such as:
Limited elevation in the eye when head is straight up
Eyes point out in a straight up gaze (divergence in up gaze)
Widening of the eyelids in the affected eye on adduction
Head tilts backwards (compensatory chin elevation to avoid double vision)
Near normal elevation in abductionHe concluded that all of these features of Brown syndrome were due to the shortening or tightening of the anterior superior oblique tendon.
A 3 mg/day dosage of DES has been associated with an incidence of thromboembolism of 9.6 to 17%, with an incidence of cardiovascular complications of 33.3%. A lower dosage of 1 mg/day DES has been associated with a rate of death due to cardiovascular events of 14.8% (relative to 8.3% for orchiectomy alone). Other long-term effects
DES has been linked to a variety of long-term adverse effects, such as increased risk of 

vaginal clear-cell adenocarcinoma
vaginal adenosis
T-shaped uterus
uterine fibroids
cervical weakness
breast cancer
infertility
hypogonadism
intersexual gestational defects
depression,
and others,in women who were treated with it during pregnancy, and/or in their offspring.A comprehensive animal study in 1993 found a plethora of adverse effects from DES such as (but not limited to) 

genotoxicity (due to quinone metabolite)
teratogenicity
penile and testicular hypoplasia
cryptorchidism (in rats and rhesus monkeys),
liver and renal cancer (in hamsters), ovarian papillary carcinoma (in canines), and
malignant uterine mesothelioma (in squirrel monkeys). Evidence was also found linking ADHD to F2 generations, demonstrating that there is at least some neurological and transgenerational effects in addition to the carcinogenic.Rodent studies reveal female reproductive tract cancers and abnormalities reaching to the F2 generation, and there is evidence of adverse effects such as irregular menstrual cycles intersexual in grandchildren of DES mothers. Additionally, evidence also points to transgenerational effects in F2 sons, such as hypospadias. At this time however, the extent of DES transgenerational effects in humans is not fully understood. Overdose
DES has been assessed in the past in clinical studies at extremely high doses of as much as 1,500 to 5,000 mg/day.