However, whether the extent of CYP3A4/5 induction at therapeutic doses reaches clinical significance is unclear. Furthermore, for example phenytoin and phenobarbital are known to reduce plasma levels of licarbazepine through induction of Cytochrome P450 enzymes. Pharmacology
Oxcarbazepine is a prodrug, which is largely metabolized to its pharmacologically active 10-monohydroxy derivative licarbazepine (sometimes abbreviated MHD). Oxcarbazepine and MHD exert their action by blocking voltage-sensitive sodium channels, thus leading to the stabilization of hyper-excited neural membranes, suppression of repetitive neuronal firing and diminishment propagation of synaptic impulses. Furthermore, anticonvulsant effects of these compounds could be attributed to enhanced potassium conductance and modulation of high-voltage activated calcium channels. Pharmacokinetics
Oxcarbazepine has high bioavailability upon oral administration. In a study in humans, only 2% of oxcarbazepine remained unchanged, 70% were reduced to licarbazepine; the rest were minor metabolites. The half-life of oxcarbazepine is considered to be about 2 hours, whereas licarbazepine has a half-life of nine hours. Through its chemical difference to carbamazepine metabolic epoxidation is avoided, reducing hepatic risks. Licarbazepine is metabolised by conjugation with Glucuronic acid. Approximately 4% are oxidised to the inactive 10,11-dihydroxy derivative. Elimination is almost completely renal, with faeces accounting to less than 4%. 80% of the excreted substances are to be attributed to licarbazepine or its glucuronides. Pharmacodynamics
Both oxcarbazepine and licarbazepine were found to show anticonvulsant properties in seizure models done on animals. These compounds had protective functions whenever tonic extension seizures were induced electrically, but such protection was less apparent whenever seizures were induced chemically.
AAOx3 is not a concerning response since people are sometimes less aware of the situation due to pain, time of day, or lack of significant event.Alternately, the letters in AAOx4 can be documented as COAX4. A person who is COAx4 is said to be "conscious, alert, & oriented to person, place, time and event". When a handoff report is made, anything less than 4 is specifically noted for clarity (e.g., patient is COAx2, oriented to self and place). Mental orientation is closely related, and often intermixed with trauma shock, including physical shock (see: Shock (circulatory)) and mental shock (see: Acute stress reaction, a psychological condition in response to terrifying events.) The exact cerebral region involved in orientation is uncertain, but lesions of the brain stem and the cerebral hemispheres have been reported to cause disorientation, suggesting that they act together in maintaining awareness and its subfunction of orientation. Disorientation
Disorientation is the opposite of orientation. It is a cognitive disability in which the senses of time, direction, and recognition of items (things), people and places become difficult to distinguish/identify. Causes of mental disorientation
Disorientation can occur in healthy young adults as well as in the elderly or ill person. While exercising, if a person becomes dehydrated as a result of over-exertion, he or she may become disoriented to the time or place. While exercising, the body may not be able to supply enough oxygen to the brain fast enough.