Jan-Pieter Teunisse

Central Coherence and Cognitive Shifting in Relation to Social Improvement in High-Functioning Young Adults with Autism

The objective of this prospective study was to evaluate the possible role of two cognitive styles – weak central coherence and poor cognitive shifting – in predicting social improvement in patients with autistic disorder. Thirty patients, largely similar in age (young adults), intelligence (high-functioning) and living conditions (residential treatment in the same unit) were assessed at two separate time points with a 3-year interval between pretest and posttest. At pretest central coherence, cognitive shifting and several aspects of social functioning – symptom severity, social intelligence and social competence – were measured. At posttest social functioning was reassessed. Unlike central coherence, cognitive shifting was identified as a significant prognostic marker. This differential outcome might be an indication that patients with poor cognitive shifting and patients with weak central coherence have different prognoses with the current, highly structured treatment milieu; it is unknown whether patients with poor cognitive flexibility might benefit more from treatments specifically designed to address this problem.

Neural Correlates of Language Comprehension in Autism Spectrum Disorders: When Language Conflicts with World Knowledge.

In individuals with ASD, difficulties with language comprehension are most evident when higher-level semantic-pragmatic language processing is required, for instance when context has to be used to interpret the meaning of an utterance. Until now, it is unclear at what level of processing and for what type of context these difficulties in language comprehension occur. Therefore, in the current fMRI study, we investigated the neural correlates of the integration of contextual information during auditory language comprehension in 24 adults with ASD and 24 matched control participants. Different levels of context processing were manipulated by using spoken sentences that were correct or contained either a semantic or world knowledge anomaly. Our findings demonstrated significant differences between the groups in inferior frontal cortex that were only present for sentences with a world knowledge anomaly. Relative to the ASD group, the control group showed significantly increased activation in left inferior frontal gyrus (LIFG) for sentences with a world knowledge anomaly compared to correct sentences. This effect possibly indicates reduced integrative capacities of the ASD group. Furthermore, world knowledge anomalies elicited significantly stronger activation in right inferior frontal gyrus (RIFG) in the control group compared to the ASD group. This additional RIFG activation probably reflects revision of the situation model after new, conflicting information. The lack of recruitment of RIFG is possibly related to difficulties with exception handling in the ASD group.

Flexibility in children with autism spectrum disorders (ASD): Inconsistency between neuropsychological tests and parent-based rating scales.

In this study, we compared neuropsychological tests and parent-based ratings of flexibility in a sample of children with autism spectrum disorders (ASD). We investigated the discriminant validity of the domain-specific flexibility measures by comparison with the domain general measures, general behavioral problems, general ASD-related traits, and general intelligence. Tests and parent-based ratings of flexibility were not significantly correlated. Parent-based ratings were strongly related with the three broadband measures, whereas the discriminant validity indices of the neuropsychological tests were satisfactory. These findings suggest that parent-based ratings do not reflect the specific executive construct of flexibility, but instead reflect a broad spectrum of general child characteristics.

One hundred years of Alzheimer's disease and the neglected second lesson of Aloïs Alzheimer on multicausality in dementia.

Alzheimer, the famous German neuropathologist and psychiatrist, wrote a preliminary report of his findings of plaques and tangles in a case of presenile dementia. This year is celebrated as the birth and recognition of a disease of still-rising importance. However, Alzheimer provided important further details on this disease in the following years. In his second lesson on Alzheimer’s disease (AD), he warned that the pathophysiology in AD usually is far more complex than to be attributed to just plaques and tangles. This second lesson is largely neglected. In the decades after 1906, and in fact during the whole twentieth century, AD became the exponent of the leading paradigm of monocausality in dementia. The single name, “Alzheimer’s disease,” underlined the leading idea that in each individual the dementia syndrome was caused by one single disease entity, with its own pathogenesis. However, from 1907 onward, and neglected by mainstream neuroscientists, some controversy about the etiology and the nosological classification of the dementias existed. In fact, right from the construction of the AD entity, Aloïs Alzheimer was already hesitant to have his name associated with the presenile dementia he described in Auguste D. as a hallmark of the uniqueness of the pathophysiology of her disease. His hesitation was fuelled by two scientific questions. First, he doubted whether the presenile dementia of Auguste D. really had a different etiology from the more prevalent cases of senile dementia. Secondly, doubt arose from another case, the 56-year-old Johann F. This patient was admitted to the university psychiatric clinic in Munich on September 12, 1907, and died there on October 3, 1910. In his 1911 work on this case, Alzheimer interpreted this patient as an atypical case of senile dementia. At a cellular level, he reported the degeneration of the smaller cerebral blood vessels, a process also referred to as Alzheimer’s sclerosis. Alzheimer questioned whether he should call the cooccurrence of plaques and tangles and vascular pathology in this patient’s brain typical or atypical for AD. He chose for this case the label of atypical Alzheimer’s dementia. Here, we will further address Alzheimer’s scientific questions on the role of aging in dementia and on monoor multicausality, which he formulated based on his second case. After 100 years, it is time to rediscover Alzheimer’s second lesson in dementia, as