More Audiologists Performing Cerumen Management
Cerumen management is on the rise among audiologists,
according to survey results published in the June 2013 issue of the American
Journal of Audiology. But respondents also reported that
they were not trained adequately enough in cerumen management, and believe that
educational programs need to improve their coverage of the subject.
Cerumen management is within the scope of practice of
audiology, and the audiology doctorate is now the entry-level clinical degree.
However, there is little recent information about whether and how cerumen
management is being taught in AuD programs—or even if and how audiologists are
currently practicing cerumen management. This study surveyed audiologists about
their training for, experience with, opinions about and practices involving
cerumen management.
Researchers designed and e-mailed a questionnaire to 1,575
audiologists with AuD degrees, randomly sampled from the American Academy of
Audiology's membership directory. The return rate was 29 percent (447 returned). Overall, 69 percent of audiologists performed cerumen management, compared to only 29 percent reported in earlier studies. More audiologists in private practice (87 percent) performed cerumen management than those in medical settings (65 percent). Almost half (48 percent) of the audiologists who had completed residential AuD programs believed that their training programs inadequately prepared them to perform cerumen management.
In Story Retelling, Children With Autism Show Qualitative
Differences
Facial and vocal expressions of people with high-functioning
autism were as recognizable as those of their typically developing peers but
were qualitatively different, according to a study published in the June 2013
issue of the Journal of Speech, Language, and Hearing Research. These preliminary data show qualitative
differences in nonverbal communication that may have a significant, negative
impact on the social communication success of children and adolescents with
high-functioning autism.
People with high-functioning autism have qualitative
differences in facial expression and prosody production, which are rarely
systematically quantified. Researchers qualitatively and quantitatively
analyzed prosody and facial expression productions in 22 male children and
adolescents with high-functioning autism and 18 typically developing controls
(17 males, 1 female). The authors used a story-retelling task to elicit
emotionally laden narratives, which they analyzed using acoustic measures and
perceptual codes. Naive listeners coded all productions for emotion type,
degree of expressiveness and awkwardness.
The group with high-functioning autism was not significantly
different in accuracy or expressiveness of facial productions, but was more
awkward than the typically developing group. Participants with high-functioning
autism were significantly more expressive in their vocal productions, with a
trend for greater awkwardness. Researchers found that more severe social
communication impairment, as captured by the Autism Diagnostic Observation
Schedule, was correlated with greater vocal and facial awkwardness.
Mystery of EEC Syndrome's Variable Severity in Children Solved
By identifying a protein that acts as a genetic modifier,
researchers have solved the mystery of why some infants are born with a grave
syndrome consisting of cleft palate and major deformities of the skin and
limbs, while other infants bearing the same predisposing genetic mutation bear
little or no sign of the illness, called EEC. The results, published online
June 14 in the American Journal of Medical Genetics,
suggest that the presence or absence of a single protein determines whether or
not a child with the mutation will develop EEC pathology.
EEC stands for ectodactyly, ectodermal dysplasia, clefting
syndrome. It is rare in its full-blown form, although individual aspects of the
associated pathology, such as cleft palate, are more common. EEC has a known
genetic culprit, a DNA mutation in a gene called p63 that causes a mutation in
the p63 protein. Only one parent needs to contribute the defective copy of the
gene for a child to develop the illness. When one parent carries the mutant
gene, each child has a 50 percent chance of having EEC.
The question is why some children with the mutation have
severe birth defects, while others—in some cases, siblings of those
affected—with the same mutation are mostly or entirely symptom-free. Genetic
experiments revealed that the presence or absence of one variant type of the
p63 protein—called TAp63—determines whether or not a child with the p63
mutation will develop EEC pathology. TAp63 normally protects from the birth
defects; the experiments showed that in its absence, pathology is certain to
occur.
The results suggest that levels of the TAp63 protein
determine whether children with one copy of the EEC-causing mutation are born
with birth defects, and that when levels of TAp63 drop beneath a certain
threshold, it is no longer protective, opening the way to pathology.