Individual differences in discounting curves are affected by personality characteristics such as self-reports of impulsivity and locus of control; personal characteristics such as age, gender, IQ, race, and culture; socioeconomic characteristics such as income and education; and many other variables. to drug addiction. Lesions of the nucleus accumbens core subregion or basolateral amygdala produce shifts towards choosing the smaller-sooner reward, suggesting the involvement of these brain regions in the preference for delayed reinforcers. There is also evidence that the orbitofrontal cortex is involved in delay discounting, although there is currently debate on whether lesions in this region result in more or less impulsivity.Economic theory suggests that optimal discounting involves the exponential discounting of value over time. This model assumes that people and institutions should discount the value of rewards and punishments at a constant rate according to how delayed they are in time. While economically rational, recent evidence suggests that people and animals do not discount exponentially. Many studies suggest that humans and animals discount future values according to a hyperbolic discounting curve where the discount factor decreases with the length of the delay (for example, waiting from today to tomorrow involves more loss of value than waiting from twenty days to twenty-one days). Further evidence for non-constant delay discounting is suggested by the differential involvement of various brain regions in evaluating immediate versus delayed consequences.
Aspirin displaces bilirubin from serum albumin, thus generating an increased level of free bilirubin which can cross the developing blood brain barrier. This can be life-threatening.Bilirubin is known to accumulate in the gray matter of neurological tissue where it exerts direct neurotoxic effects. It appears that its neurotoxicity is due to mass-destruction of neurons by apoptosis and necrosis. Risk factors
Premature birth
Rh incompatibility
Polycythemia – often present in neonates
Sulfonamides (e.g. co-trimoxazole) – displaces bilirubin from serum albumin
Crigler–Najjar syndrome, type I
G6PD deficiency
BruisingGilberts syndrome and G6PD deficiency occurring together especially increases the risk for kernicterus. Diagnosis
In neonates with kernicterus, the Moro reflex may be absent or symmetrically reduced. Prevention
Measuring the serum bilirubin is helpful in evaluating a babys risk for developing kernicterus. These numbers can then be plotted on the Bhutani nomogram. In neonates with hyperbilirubinemia, light therapy may be effective in reducing the serum bilirubin level. More severe cases may require the use of exchange transfusion. Treatment
Currently no effective treatment exists for kernicterus. Future therapies may include neuroregeneration. A handful of patients have undergone deep brain stimulation, and experienced some benefit. Drugs such as baclofen, clonazepam, gabapentin, and artane are often used to manage movement disorders associated with kernicterus. Proton pump inhibitors are also used to help with reflux. Cochlear implants and hearing aids have also been known to improve the hearing loss that can come with kernicterus (auditory neuropathy – ANSD). Notable people
Claudio Tiribelli, Italian hepatologist, studies on Kernicterus

References


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