British authorities banned the term shell shock during World War II to avoid an epidemic of cases, and the term posttrauma concussion state was coined in 1939 to describe "disturbance of consciousness with no immediate or obvious pathologic change in the brain". The term postconcussion syndrome was in use by 1941.In 1961, H. Miller first used the term "accident neurosis" to refer to the syndrome which is now called PCS and asserted that the condition only occurs in situations where people stand to be compensated for the injury. The real causes of the condition remain unclear. Controversy
Though no universally accepted definition of postconcussive syndrome exists, most of the literature defines the syndrome as the development of at least three of the following symptoms: headache, dizziness, fatigue, irritability, impaired memory and concentration, insomnia, and lowered tolerance for noise and light. One complication in diagnosis is that symptoms of PCS also occur in people who have no history of head injury, but who have other medical and psychological complaints. In one study 64% of people with TBI, 11% of those with brain injuries, and 7% of those with other injuries met the DSM-IV criteria for post-concussion syndrome. Many of these individuals with PCS were misdiagnosed as having other unrelated conditions due to commonality of symptoms. (see diagnosis above).Headache is one of the criteria for PCS, but it is notably undetermined where the headache comes from.
Cutis laxa may also be seen in association with inherited connective tissue disorders such as Ehlers–Danlos syndromes. Another syndrome associated with cutis laxa is Lenz-Majewski syndrome which is due to a mutation in the phosphatidylserine synthase 1 (PTDSS1) gene.In contrast, acquired cutis laxa often has a triggering event such as urticaria, drugs (such as penicillin) or neoplasms. Acquired cutis laxa may also be immunologically mediated, as it can involve dermal deposit of immunoglobulins and it can occur with autoimmune diseases. Acquired cutis laxa has been associated with granular immunoglobulin A deposits as well as abundant neutrophils. One hypothesis for the cause is excessive elastase release from neutrophils and macrophages. It has also been considered that mutations in elastin (ELN) and fibulin-5 (FBLN5) genes can increase susceptibility of elastic fibres to inflammatory degradation in acquired cutis laxa.Acquired cutis laxa has also been seen in conjunction with a number of conditions including: rheumatoid arthritis, systemic lupus erythematosus, celiac disease, and monoclonal gammopathies. It can also occur as a postinflammatory response after urticaria. Urticarial skin fibroblasts have shown a 2- to 3- fold increase in elastase activity in a patient with acquired cutis laxa. Diagnosis
Treatment
As of 2019, there is no treatment for cutis laxa. Procedures aimed at mitigating symptoms and identifying subsequent conditions are often advised. No pharmacological  agent has been able to stop the progression of the disease. However, cosmetic surgeries are potentially an option as cutis laxa does not generally involve vascular fragility. See also
Occipital horn syndrome
List of cutaneous conditions

References
Further reading
External links

Medscape entry on Cutis Laxa