Combat stress reaction (CSR) is acute behavioral disorganization as a direct result of the trauma of war. Also known as "combat fatigue", "battle fatigue", or "battle neurosis", it has some overlap with the diagnosis of acute stress reaction used in civilian psychiatry. It is historically linked to shell shock and can sometimes precurse post-traumatic stress disorder. Combat stress reaction is an acute reaction that includes a range of behaviors resulting from the stress of battle that decrease the combatants fighting efficiency. The most common symptoms are fatigue, slower reaction times, indecision, disconnection from ones surroundings, and the inability to prioritize. Combat stress reaction is generally short-term and should not be confused with acute stress disorder, post-traumatic stress disorder, or other long-term disorders attributable to combat stress, although any of these may commence as a combat stress reaction. The US Army uses the term/acronym COSR (Combat Stress Reaction) in official medical reports. This term can be applied to any stress reaction in the military unit environment. Many reactions look like symptoms of mental illness (such as panic, extreme anxiety, depression, and hallucinations), but they are only transient reactions to the traumatic stress of combat and the cumulative stresses of military operations.In World War I, shell shock was considered a psychiatric illness resulting from injury to the nerves during combat. The horrors of trench warfare meant that about 10% of the fighting soldiers were killed (compared to 4.5% during World War II) and the total proportion of troops who became casualties (killed or wounded) was about 57%.
8p23.1 duplication syndrome is a rare genetic disorder caused by a duplication of a region from human chromosome 8. This duplication syndrome has an estimated prevalence of 1 in 64,000 births  and is the reciprocal of the 8p23.1 deletion syndrome. The 8p23.1 duplication is associated with a variable phenotype including one or more of speech delay, developmental delay, mild dysmorphism, with prominent forehead and arched eyebrows, and congenital heart disease (CHD). Presentation
The phenotypic data on 11 patients indicated that cases are not always ascertained for CHD but that CHD was the most common single feature found in 6 out of 11 individuals. Developmental delay and/or learning difficulties were found in 5 out of 11 cases, but one prenatal case was developing normally at 15 months of age (Case 1,). Three other prenatal cases could not yet be reliably assessed. A variable degree of facial dysmorphism was present in 5 out of 11 individuals. Partial toe syndactyly has been found in one mother and son diad and adrenal anomalies in two probands but not in the duplicated mother of one of them. The phenotype is compatible with independent adult life with varying degrees of support. Duplication of the GATA4 transcription factor (OMIM: 600576) is believed to underlie the congenital heart disease and other genes, common to the duplication and deletion syndromes, can be regarded as candidates for the 8p23.1 duplication syndrome. These include the SOX7 transcription factor (OMIM: 612202) for both CHD and developmental delay  and the TNKS gene (OMIM: 603303) for behavioural difficulties.