Research into puerperal mania is, therefore, not the study of a disease-in-its-own right, but an investigation into the childbearing triggers of bipolar disorder. Psychoses triggered in the first two weeks after the birth – between the first postpartum day (or even during parturition  until about the 15th day – complicate approximately 1/1,000 pregnancies. The impression is sometimes given that this is the only trigger associated with childbearing. But there is evidence of four other triggers – late postpartum, prepartum, post-abortion  and weaning. Marcé, widely considered an authority on puerperal psychoses, claimed that they could be divided into early and late forms; the late form begins about six weeks after childbirth, associated with the return of the menses. His view is supported by the large number of cases in the literature with onset 4–13 weeks after the birth, mothers with serial 4-13 week onsets and some survey evidence. The evidence for a trigger acting in pregnancy is also based on the large number of reported cases, and particularly on the frequency of mothers experiencing two or more prepartum episodes. There is evidence, especially from surveys, of bipolar episodes triggered by abortion (miscarriage or termination). The evidence for a weaning trigger rests on 32 cases in the literature, of which 14 were recurrent. The relative frequency of these five triggers is given by the number of cases in the literature – just over half early postpartum onset, 20% each late postpartum and prepartum onset, and the rest post-abortion and weaning onset.
Superior oblique myokymia is a neurological disorder affecting vision and was named by Hoyt and Keane in 1970.It is a condition that presents as repeated, brief episodes of movement, shimmering or shaking of the vision of one eye, a feeling of the eye trembling, or vertical/tilted vision. It can present as one or more of these symptoms. Diagnosis is most often made by the elimination of other conditions, disorders or diseases. Onset usually occurs in adulthood, and the course is benign and is not commonly associated with other disorders. Causes
In 1983, Bringewald postulated that superior oblique myokymia resulted from vascular compression of the trochlear nerve (fourth cranial nerve), which controls the action of the superior oblique muscle in the eye. By 1998, there had been only one reported case of compression of the trochlear nerve by vessels. More recently, magnetic resonance imaging experiments have shown that neurovascular compression at the root exit zone of the trochlear nerve can result in superior oblique myokymia. Diagnosis
Treatment
Treatment can include pharmaceutical or surgical means. The drug carbamazepine (Tegretol) has been used successfully. Other drugs with variable success include gabapentin and, recently, memantine. Successful surgery options include superior oblique tenectomy accompanied by inferior oblique myectomy. However, "[o]verall, the bulk of the ophthalmic literature would agree with the viewpoint that invasive craniotomy surgical procedures should be justified only by the presence of intractable and absolutely unbearable symptoms. "Samii et al. and Scharwey and Samii described a patient who had superior oblique myokymia for 17 years.