Neuro-obstetrics: A multidisciplinary approach to care of women with neurologic disease.

The term "neuro-obstetrics" refers to a multidisciplinary approach to the care of pregnant women with neurologic comorbidities, both preconceptionally and throughout pregnancy. General preconception care should be offered to all women, including women with neurologic disease. Women with neurologic comorbidities should also be offered specialist preconception care by an obstetrician who consults with a neurologist, anesthesiologist, and if indicated clinical geneticist and/or other specialists. In women with neurologic comorbidities, neurologic sequelae may influence the course of the pregnancy and delivery. Also, pregnancy may influence the severity of the neurologic condition, depending on the type of disease. Physiologic adaptations during pregnancy and altered pharmacokinetics may cause altered blood serum levels of drugs, leading to decreased or increased drug effects. When administering drugs to a woman who wishes to conceive, it is important to consider possible teratogenic effects and possible secretion in breast milk. Tailoring medication regimens should be considered, preferably preconceptionally. In this chapter, we review general principles of neuro-obstetric care, as well as some specific considerations for neurologists, obstetricians, and anesthesiologists caring for pregnant women with common neurologic conditions.

Brain microvasculature defects and Glut1 deficiency syndrome averted by early repletion of the glucose transporter-1 protein.

Haploinsufficiency of the SLC2A1 gene and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1 DS. We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting in a profound diminution of the brain microvasculature without compromising the blood-brain barrier. Studies to define the temporal requirements for Glut1 reveal that pre-symptomatic, AAV9-mediated repletion of the protein averts brain microvasculature defects and prevents disease, whereas augmenting the protein late, during adulthood, is devoid of benefit. Still, treatment following symptom onset can be effective; Glut1 repletion in early-symptomatic mutants that have experienced sustained periods of low brain glucose nevertheless restores the cerebral microvasculature and ameliorates disease. Timely Glut1 repletion may thus constitute an effective treatment for Glut1 DS.