Hand function does not seem to have similar declines. Chronic disease risk, such as obesity, is also higher among adults with cerebral palsy than the general population. Common problems include increased pain, reduced flexibility, increased spasms and contractures, post-impairment syndrome and increasing problems with balance. Increased fatigue is also a problem. When adulthood and cerebral palsy is discussed, as of 2011, it is not discussed in terms of the different stages of adulthood.Like they did in childhood, adults with cerebral palsy experience psychosocial issues related to their CP, chiefly the need for social support, self-acceptance, and acceptance by others. Workplace accommodations may be needed to enhance continued employment for adults with CP as they age. Rehabilitation or social programs that include salutogenesis may improve the coping potential of adults with CP as they age. Epidemiology
Cerebral palsy occurs in about 2.1 per 1000 live births. In those born at term rates are lower at 1 per 1000 live births. Within a population it may occur more often in poorer people. The rate is higher in males than in females; in Europe it is 1.3 times more common in males.There was a "moderate, but significant" rise in the prevalence of CP between the 1970s and 1990s. This is thought to be due to a rise in low birth weight of infants and the increased survival rate of these infants.
Opioids and especially benzodiazepines also increase the risk of potentially lethal respiratory depression.Strong inhibitors of the liver enzyme CYP3A4, such as ketoconazole, moderately increase buprenorphine concentrations; CYP3A4 inducers can theoretically decrease concentrations of buprenorphine. Pharmacology
Mechanism of action
Buprenorphine binds strongly to opioid receptors and acts as a pain-reducing medication in the central nervous system (CNS). It binds to the μ-opioid receptor with high affinity, which produces the analgesic effects in the CNS. It is a partial μ-opioid receptor agonist and a weak κ-opioid receptor antagonist. As the dose of buprenorphine increases, its analgesic effects reach a plateau, and then it starts to act like an antagonist. As a partial agonist, buprenorphine binds and activates the opioid receptors, but has only partia  efficacy at the receptor relative to a full agonist, even at maximal receptor occupancy. It is thus well-suited to treat opioid dependence, as it produces milder effects on the opioid receptor with lower dependence and habit-forming potential. Naloxone is a pure opioid antagonist that competes with opioid molecules in the CNS and prevents them from binding to the opioid receptors. Naloxones binding affinity is highest for the μ-opioid receptor, then the δ-opioid receptor, and lowest for the κ-opioid receptor. Naloxone has poor bioavailability, and is rapidly inactivated following oral administration. When injected, it exerts its full effects. The principle behind its function as a deterrent is as follows: when taken sublingually as prescribed, buprenorphines effects at the opioid receptor dominate, while naloxones effects are negligible due to the low oral absorption.