These ADME abnormalities, it is also suggested, may interact with particular HLA proteins and T cell receptors to promote a SCARs disorder. Diagnosis
The diagnosis is based on involvement of less than 10% of the skin. It is known as TEN when more than 30% of the skin is involved and an intermediate form with 10 to 30% involvement. A positive Nikolskys sign is helpful in the diagnosis of SJS and TEN. A skin biopsy is helpful, but not required, to establish a diagnosis of SJS and TEN. Pathology
SJS, like TEN and erythema multiforme, is characterized by confluent epidermal necrosis with minimal associated inflammation. The acuity is apparent from the (normal) basket weave-like pattern of the stratum corneum. Classification
Stevens–Johnson syndrome (SJS) is a milder form of toxic epidermal necrolysis (TEN). These conditions were first recognised in 1922. A classification first published in 1993, that has been adopted as a consensus definition, identifies Stevens–Johnson syndrome, toxic epidermal necrolysis, and SJS/TEN overlap. All three are part of a spectrum of severe cutaneous reactions (SCAR) which affect skin and mucous membranes. The distinction between SJS, SJS/TEN overlap, and TEN is based on the type of lesions and the amount of the body surface area with blisters and erosions. It is agreed that the most reliable method to classify EM, SJS, and TEN is based on lesion morphology and extent of epidermal detachment. Blisters and erosions cover between 3% and 10% of the body in SJS, 11–30% in SJS/TEN overlap, and over 30% in TEN.
Both are the inability to plan volitional motor movements for speech production in the absence of muscular weakness. Apraxia is not a result of sensory problems, or physical issues with the articulatory structures themselves, simply the way the brain plans to move them. Developmental verbal dyspraxia
Developmental verbal dyspraxia is a developmental inability to motor plan volitional movement for the production of speech in the absence of muscular weakness. Research has suggested links to the FOXP2 gene. See also
KE family

References

Duffy, Joseph (2013), Motor speech disorders (3rd ed. ), St. Louis, MO: Elsevier Mosby