These brain regions are all parts of the limbic system, which is heavily involved in emotion and memory. KS involves neuronal loss, that is, damage to neurons; gliosis, which is a result of damage to supporting cells of the central nervous system, and bleeding also occurs in mammillary bodies. Damage to the medial dorsal nucleus or anterior nuclei of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/or structural damage in the diencephalon.Originally, it was thought that a lack of initiative and a flat affect were important characteristics of emotional presentation in those affected. Studies have questioned this, proposing that neither is necessarily a symptom of KS. Research suggesting that people with Korsakoff syndrome are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which is a usual characteristic, reflects a deficit of emotional expressions, without affecting the experience or perception of emotion.KS causes deficits in declarative memory in most people, but leaves implicit spatial, verbal, and procedural memory functioning intact. People with KS have deficits in the processing of contextual information. Context memories refers to the where and when of experiences, and is an essential part of recollection. The ability to store and retrieve this information, such as spatial location or temporal order information, is impaired. Research has also suggested that people with Korsakoff syndrome have impaired executive functions, which can lead to behavioral problems and interfere with daily activities.
Table 11–2)
but these anomalies include:

gastrointestinal abnormalities such as esophageal atresia and duodenal atresia (causing inability to swallow amniotic fluid), anencephaly, facial cleft, neck masses, tracheoesophageal fistula, and diaphragmatic hernias. An annular pancreas causing obstruction may also be the cause. Bochdaleks hernia, in which the pleuro-peritoneal membranes (especially the left) will fail to develop and seal the pericardio-peritoneal canals. This results in the stomach protrusion up into the thoracic cavity, and the fetus is unable to swallow sufficient amounts of amniotic fluid. fetal renal disorders that result in increased urine production during pregnancy, such as in antenatal Bartter syndrome. Molecular diagnosis is available for these conditions. neurological abnormalities such as anencephaly, which impair the swallowing reflex. Anencephaly is failure of closure of the rostral neuropore (rostral neural tube defect). If the rostral neuropore fails to close there will be no neural mechanism for swallowing. chromosomal abnormalities such as Down syndrome and Edwards syndrome, which is itself often associated with gastrointestinal abnormalities. Skeletal dysplasia, or dwarfism. There is a possibility of the chest cavity not being large enough to house all of the babys organs causing the trachea and esophagus to be restricted, not allowing the baby to swallow the appropriate amount of amniotic fluid. sacrococcygeal teratoma

Diagnosis
There are several pathologic conditions that can predispose a pregnancy to polyhydramnios. These include a maternal history of diabetes mellitus, Rh incompatibility between the fetus and mother, intrauterine infection, and multiple pregnancies. During the pregnancy, certain clinical signs may suggest polyhydramnios.