Why some proteins do not denature and subsequently trigger allergic reactions and hypersensitivity while others do is not entirely clear.Hypersensitivities are categorized according to the parts of the immune system that are attacked and the amount of time it takes for the response to occur. The four types of hypersensitivity reaction are:  type 1, immediate IgE-mediated; type 2, cytotoxic; type 3, immune complex-mediated; and type 4, delayed cell-mediated. The pathophysiology of allergic responses can be divided into two phases. The first is an acute response that occurs immediately after exposure to an allergen. This phase can either subside or progress into a "late-phase reaction" which can substantially prolong the symptoms of a response, and result in tissue damage.Many food allergies are caused by hypersensitivities to particular proteins in different foods. Proteins have unique properties that allow them to become allergens, such as stabilizing forces in their tertiary and quaternary structures which prevent degradation during digestion. Many theoretically allergenic proteins cannot survive the destructive environment of the digestive tract, thus do not trigger hypersensitive reactions. Acute response
In the early stages of allergy, a type I hypersensitivity reaction against an allergen, encountered for the first time, causes a response in a type of immune cell called a TH2 lymphocyte, which belongs to a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These TH2 cells interact with other lymphocytes called B cells, whose role is the production of antibodies.
The International League Against Epilepsy (ILAE) in 2011 recommended abandoning these terms for reasons of clarity and instead trying to place individual cases into one of the following three groups: genetic, structural/metabolic, and unknown. The new terms are more immediately clear in their meaning, except that the structural and metabolic group includes cases that have a genetic component that does not always directly lead to the condition. Only the genetic grouping has a known direct genetic cause. "Unknown" cases may be of unknown genetic, structural, metabolic, or other unknown cause.The old terminology was defined by the ILAE as follows:
symptomatic:  the epilepsy is the consequence of a known or suspected disorder of the central nervous system. cryptogenic: this refers to a disorder whose cause is hidden or occult. Cryptogenic epilepsies are presumed to be symptomatic. idiopathic:  there is no underlying cause other than a possible hereditary predisposition.The remainder of this section will refer to the older terminology. Symptomatic
If a cause presents itself, the syndrome is referred to as symptomatic West syndrome, as the attacks manifest as a symptom of another problem. Almost any cause of brain damage could be associated, and these are divided into prenatal, perinatal, and post-natal. The following is a partial list:
In around one third of the children, there is evidence of a profound organic disorder of the brain. This includes:microcephaly
cortical dysplasia
cerebral atrophy
lissencephaly
bacterial meningitis
phakomatoses (e.g. tuberous sclerosis)
Aicardi syndrome
cephalhematoma and
vascular malformation. Furthermore, other causes increasingly being named in the literature are:
Incontinentia pigmenti
Foix–Chavany–Marie syndrome
Patau syndrome (trisomy 13)
Sturge–Weber syndrome
neurometabolic diseases
congential infections (e.g.