Furthermore, a hearing loss may exist in only one ear (unilateral) or in both ears (bilateral). Hearing loss can be temporary or permanent, sudden or progressive. The severity of a hearing loss is ranked according to ranges of nominal thresholds in which a sound must be so it can be detected by an individual. It is measured in decibels of hearing loss, or dB HL. There are three main types of hearing loss: conductive hearing loss, sensorineural hearing loss, and mixed hearing loss. An additional problem which is increasingly recognised is auditory processing disorder which is not a hearing loss as such but a difficulty perceiving sound. The shape of an audiogram shows the relative configuration of the hearing loss, such as a Carhart notch for otosclerosis, noise notch for noise-induced damage, high frequency rolloff for presbycusis, or a flat audiogram for conductive hearing loss. In conjunction with speech audiometry, it may indicate central auditory processing disorder, or the presence of a schwannoma or other tumor. People with unilateral hearing loss or single-sided deafness (SSD) have difficulty in hearing conversation on their impaired side, localizing sound, and understanding speech in the presence of background noise. One reason for the hearing problems these patients often experience is due to the head shadow effect. Prevention
It is estimated that half of cases of hearing loss are preventable. About 60% of hearing loss in children under the age of 15 can be avoided.
Although most individuals with kernicteric cerebral palsy have normal intelligence, some children with mild choreoathetosis develop dull normal intelligence or mild intellectual disability even without auditory dysfunction. Causes
In the vast majority of cases, kernicterus is associated with unconjugated hyperbilirubinemia during the neonatal period. The blood–brain barrier is not fully functional in neonates and therefore bilirubin is able to cross into the central nervous system. Moreover, neonates have much higher levels of bilirubin in their blood due to:

Rapid breakdown of fetal red blood cells immediately prior to birth, with subsequent replacement by normal adult human red blood cells. This breakdown of fetal red blood cells releases large amounts of bilirubin. Severe hemolytic disease of the newborn. Many children who survive exhibit permanent mental impairment or damage to motor areas of the brain because of precipitation of bilirubin in neurons. Neonates have a limited ability to metabolize and excrete bilirubin. The sole pathway for bilirubin elimination is through the uridine diphosphate glucuronosyltransferase isoform 1A1 (UGT1A1) enzyme, which performs a reaction called "glucuronidation". This reaction adds a large sugar to the bilirubin, which makes the compound more water-soluble, so it can be more readily excreted via the urine and/or the feces. The UGT1A1 enzyme is not active in appreciable amounts until several months after birth. Apparently, this is a developmental compromise since the maternal liver and placenta perform glucuronidation for the fetus. Administration of aspirin to neonates and infants.