This view has been bolstered recently by novel immunological and clinical studies that have confirmed gross aberrations in this early response, consistent with subsequent genetic studies that highlighted molecules important for innate immune function. The suggestion therefore is that Crohns pathogenesis actually results from partial immunodeficiency, a theory that coincides with the frequent recognition of a virtually identical, non-infectious inflammatory bowel disease arising in patients with congenital monogenic disorders impairing phagocyte function. Causes
While the exact cause or causes are unknown, Crohns disease seems to be due to a combination of environmental factors and genetic predisposition. Crohns is the first genetically complex disease in which the relationship between genetic risk factors and the immune system is understood in considerable detail. Each individual risk mutation makes a small contribution to the overall risk of Crohns (approximately 1:200). The genetic data, and direct assessment of immunity, indicates a malfunction in the innate immune system. In this view, the chronic inflammation of Crohns is caused when the adaptive immune system tries to compensate for a deficient innate immune system. Genetics
Crohns has a genetic component. Because of this, siblings of known people with Crohns are 30 times more likely to develop Crohns than the general population.The first mutation found to be associated with Crohns was a frameshift in the NOD2 gene (also known as the CARD15 gene), followed by the discovery of point mutations. Over 30 genes have been associated with Crohns; a biological function is known for most of them.
Acute mania
As for its efficacy in the treatment of acute mania, a recent meta-analysis showed that it produces comparatively small improvements in manic symptoms in patients with acute mania and mixed episodes than most other antipsychotic drugs (with the exception of ziprasidone) such as risperidone and olanzapine. Drop-out rates (in clinical trials) were also unusually high with asenapine. According to a post-hoc analysis of two 3-week clinical trials it may possess some antidepressant effects in patients with acute mania or mixed episodes. Adverse effects
Adverse effect incidenceVery common (>10% incidence) adverse effects include:

SomnolenceCommon (1-10% incidence) adverse effects include:

Weight gain
Increased appetite
Extrapyramidal side effects (EPS; such as dystonia, akathisia, dyskinesia, muscle rigidity, parkinsonism)
Sedation
Dizziness
Dysgeusia
Oral hypoaesthesia
Increased alanine aminotransferase
FatigueUncommon (0.1-1% incidence) adverse effects include:

Hyperglycaemia — elevated blood glucose (sugar)
Syncope
Seizure
Dysarthria
sinus bradycardia
Bundle branch block
QTc interval prolongation (has a relatively low risk for causing QTc interval prolongation.)