To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Autism encompasses wide disparities of memory and learning: at one extreme, some children with autism learn virtually no language and very little about the world around them; at the opposite extreme, other children with autism may show prodigious memorization and savant abilities. In family members of individuals with autism, unusual intellectual abilities are over-represented (DeLong, Ritch & Burch, 2002; Dor-Shav & Horowitz, 1984). Memory ability – but not cognitive profiles of visualization and reasoning – has been found to differentiate high- and low- functioning individuals with autism (Russo et al., 2005). This suggests that the most disabling cognitive aspects of low-functioning autism may be due to memory disability (and raises the question whether the common research focus on high-functioning autism may tend to obscure the role of memory in the cognitive deficits of autism).
The hippocampus has a unique role in memory and cognition – a role that is still being clarified, and is directly pertinent to autism. In this chapter a genetic hypothesis will be presented, focused on hippocampal function and bringing together many seemingly unrelated aspects of autism. The hypothesis relates to the role of the GABA(A) receptor subunit gene GABRA5. This gene, located in chromosome 15q11–13, has been closely associated with autism in genetic linkage studies (McCauley et al., 2004; Shao et al., 2003). The same gene has been associated independently with bipolar disorder, a fact that is relevant to the hypothesis to be proposed (Otani et al., 2005; Papadimitriou et al., 2001).
One hundred and twenty-nine children, 2 to 8 years old, with idiopathic autistic spectrum disorder diagnosed by standard instruments (Childhood Austim Ratings Scale and Autism Diagnostic Observation Schedule) were treated with fluoxetine (0.15 to 0.5mg/kg) for 5 to 76 months (mean 32 to 36 months), with discontinuation trials. Response criteria are described. Family histories were obtained using the family history method in repeated interviews. Fluoxetine response, family history of major affective disorder, and unusual intellectual achievement, pretreatment language, and hyperlexia were used to define a coherent subgroup of autistic spectrum disorder. Statistical analyses were post hoc. Of the children, 22 (17%) had an excellent response, 67 (52%) good, and 40 (31%) fair/poor. Treatment age did not correlate with response. Fluoxetine response correlated robustly with familial major affective disorder and unusual intellectual achievement, and with hyperlexia in the child. Family history of bipolar disorder and of unusual intellectual achievement correlated strongly. Five children developed bipolar disorder during follow-up. Fluoxetine response, family history of major affective disorder (especially bipolar), unusual achievement, and hyperlexia in the children appear to define a homogeneous autistic subgroup. Bipolar disorder, unusual intellectual achievement, and autistic spectrum disorders cluster strongly in families and may share genetic determinants.
Growth and development of 207 children (49% males; mean age 5.4 years [SD 0.2], range 4 to 7.3 years whose mothers received iodine during pregnancy, and children who received iodine first in their 2nd year, were examined in 1996; 192 children (49% males; mean age 6.5 years[SD 0.2], range 5.8 to 6.9 years) whose mothers received iodine while pregnant were seen in 1998. Children were from the southern part of China's Xinjiang Province which has the lowest levels of iodine in water and soil ever recorded. Head circumference but not height was improved for those who received iodine during pregnancy (compared with those receiving iodine at age 2) and for those supplemented before the end of the 2nd trimester (relative to those supplemented during the 3rd trimester). Iodine before the 3rd trimester predicted higher psychomotor test scores for children relative to those provided iodine later in pregnancy or at 2 years. Results from the test for cognitive development resulted in trend only differences between those children supplemented during pregnancy versus later. The results address the question of when maternal iodine supplements should begin in public health programs world wide. Findings may be relevant to the treatment of maternal and newborn thyroid deficiency in industrialized countries, particularly for those infants delivered before the end of the second trimester.
Email your librarian or administrator to recommend adding this to your organisation's collection.