Oxytocin was added to the Institute for Safe Medication Practicess list of High Alert Medications in Acute Care Settings in 2012. The list includes medications that have a high risk for harm if administered incorrectly.During pregnancy, increased uterine motility has led to decreased heart rate, cardiac arrhythmia, seizures, brain damage, and death in the fetus or neonate.Use is linked to an increased risk of postpartum depression in the mother.Certain learning and memory functions are impaired by centrally administered oxytocin. Also, systemic oxytocin administration can impair memory retrieval in certain aversive memory tasks. However, oxytocin does seem to facilitate learning and memory specifically for social information. Healthy males administered intranasal oxytocin show improved memory for human faces, in particular happy faces. Pharmacokinetics
Routes of administration
One IU of oxytocin is the equivalent of about 2 μg or mcg of pure peptide. Injection: Clinical doses of oxytocin are given by injection either into a muscle or into a vein to cause contraction of the uterus. Very small amounts (< 1%) do appear to enter the central nervous system in humans when peripherally administered. The compound has a half-life of typically about 3 minutes in the blood when given intravenously. Intravenous administration requires 40 minutes to reach a steady-state concentration and achieve maximum uterine contraction response. Buccal: Oxytocin was delivered in buccal tablets, but this is not common practice any more. Under the tongue: Oxytocin is poorly absorbed sublingually.
The lack of family history does not rule out CMT, but is helpful to rule out other causes of neuropathy, such as diabetes or exposure to certain chemicals or drugs.In 2010, CMT was one of the first diseases where the genetic cause of a particular patients disease was precisely determined by sequencing the whole genome of an affected individual. This was done by the scientists employed by the Charcot Marie Tooth Association (CMTA). Two mutations were identified in a gene, SH3TC2, known to cause CMT. Researchers then compared the affected patients genome to the genomes of the patients mother, father, and seven siblings with and without the disease. The mother and father each had one normal and one mutant copy of this gene, and had mild or no symptoms. The offspring who inherited two mutant genes presented fully with the disease. Histology
The constant cycle of demyelination and remyelination, which occurs in CMT, can lead to the formation of layers of myelin around some nerves, termed an "onion bulb". These are also seen in chronic inflammatory demyelinating polyneuropathy. Muscles show fiber type grouping, a similarly nonspecific finding that indicates a cycle of denervation/reinnervation. Normally, type I and type II muscle fibers show a checkerboard-like random distribution. However, when reinnervation occurs, the group of fibers associated with one nerve are of the same type. The standard for indicating fiber type is histoenzymatic adenosine triphosphatase (ATPase at pH 9.4). Management
Often, the most important goal for patients with CMT is to maintain movement, muscle strength, and flexibility.