This deficient mechanism is probably located at the level of the B30.2 domain (exon 10) where most of the pathogenic mutations associated with FMF are located. It is probably the interaction of this domain with the cytoskeleton (microtubules) that is failing, as suggested by the efficacy of colchicine.It is not conclusively known what exactly sets off the attacks, and why overproduction of IL-1 would lead to particular symptoms in particular organs (e.g. joints or the peritoneal cavity). Diagnosis
The diagnosis is clinically made on the basis of the history of typical attacks, especially in patients from the ethnic groups in which FMF is more highly prevalent. An acute phase response is present during attacks, with high C-reactive protein levels, an elevated white blood cell count and other markers of inflammation. In patients with a long history of attacks, monitoring the kidney function is of importance in predicting chronic kidney failure.A genetic test is also available to detect mutations in the MEFV gene. Sequencing of exons 2, 3, 5, and 10 of this gene detects an estimated 97% of all known mutations.A specific and highly sensitive test for FMF is the "metaraminol provocative test (MPT)", whereby a single 10 mg infusion of metaraminol is administered to the patient. A positive diagnosis is made if the patient presents with a typical, albeit milder, FMF attack within 48 hours. As MPT is more specific than sensitive, it does not identify all cases of FMF, although a positive MPT can be very useful.
Treatment
Anumonye reported treatment success with lorazepam; others found benefit with antidepressants and relaxation exercises. Epidemiology
BFS has been reported in other African cultures, and also in Brazil, Argentina, and Ethiopian Jews. Historic higher reported prevalence among males may be due to more males being present in higher education in African countries. Studies since the 1990s have not verified gender differences. Other studies found a possible association with low socioeconomic status, an association with average or higher intelligence, and a high association with neuroticism. Individuals with BFS have been found to have problems with isolation, poor study habits, and the use of psychostimulants as well as physical changes including in muscle tension and heart rate. History
The condition was first described by R. H. Prince who named the condition based on the term brain fag used by students who believed their symptoms were attributed to "brain fatigue". However, this term was used in the United States and Europe dating back to 1839. Furthermore, in a detailed historical account, Ayonrinde (2020) illustrates that contrary to widely held and published belief in diagnostic manuals, psychiatric, social science and educational text, the term "Brain Fag" and associated syndromes of anxiety, affective and somatoform symptoms in student and "brain worker" populations were first described in nineteenth century Britain (Tunstall, 1850) with dissemination across the British Empire. Ayonrinde concludes that, the time has come for the decolonization of brain fag and its African syndromization in the true spirit of ethical scientific rigor in the twenty-first century. See also
Burnout
Exhaustion


== References ==