"Although a neurobehavioural disorder, its underlying pathophysiology is not well understood. However, 'abnormalities' in the function of the prefrontal cortex, basal ganglia and cerebellum have been heavily implicated (Bauman et al., 1997; Sears et al., 1999; Allen et al., 2004; Hollander et al, 2005; Haznedar et al, 2006; Voelbel et al., 2006) as have a variety of neurotransmitters, including dopamine and serotonin (Makkonen et al., 2008; Nakamura et al., 2010)—both of which have been implicated in timing and time perception (Coull et al., 2008, 2011; Sysoeva et al., 2010; Meck et al., 2011; Weiner et al., 2011). Allman et al. (2011a) "
[Show abstract][Hide abstract] ABSTRACT: Distortions in time perception and timed performance are presented by a number of different neurological and psychiatric conditions (e.g. Parkinson's disease, schizophrenia, attention deficit hyperactivity disorder and autism). As a consequence, the primary focus of this review is on factors that define or produce systematic changes in the attention, clock, memory and decision stages of temporal processing as originally defined by Scalar Expectancy Theory. These findings are used to evaluate the Striatal Beat Frequency Theory, which is a neurobiological model of interval timing based upon the coincidence detection of oscillatory processes in corticostriatal circuits that can be mapped onto the stages of information processing proposed by Scalar Timing Theory.
"However, this effect appears to be age-dependent, as the most pronounced period of head/brain enlargement occurs in early postnatal periods, perhaps ages 1–4 years (Courchesne et al., 2001; Hazlett et al., 2005; Schumann et al., 2010), while this atypical enlargement is increasingly absent later in development. For example, while post-mortem brain weights for children with autism spectrum disorders are generally comparable with those of same age controls, adults with autism spectrum disorders tend to have lighter post-mortem brains than adult controls (Bauman and Kemper, 1997). Furthermore, Aylward and colleagues (2002) found that children with autism spectrum disorders of 8–12 years of age had larger brain volumes than their same-age typically developing peers, while typically developing individuals and those with autism spectrum disorders ranging in age from 12 to 46 years had comparable brain volumes. "
[Show abstract][Hide abstract] ABSTRACT: Studies of head size and brain volume in autism spectrum disorders have suggested that early cortical overgrowth may be followed by prematurely arrested growth. However, the few investigations quantifying cortical thickness have yielded inconsistent results, probably due to variable ages and/or small sample sizes. We assessed differences in cortical thickness between high-functioning adolescent and young adult males with autism spectrum disorders (n = 41) and matched typically developing males (n = 40). We hypothesized thinner cortex, particularly in frontal, parietal and temporal regions, for individuals with autism spectrum disorders in comparison with typically developing controls. Furthermore, we expected to find an age × diagnosis interaction: with increasing age, more pronounced cortical thinning would be observed in autism spectrum disorders than typically developing participants. T(1)-weighted magnetization prepared rapid gradient echo 3 T magnetic resonance imaging scans were acquired from high-functioning males with autism spectrum disorders and from typically developing males matched group-wise on age (range 12-24 years), intelligence quotient (≥ 85) and handedness. Both gyral-level and vertex-based analyses revealed significantly thinner cortex in the autism spectrum disorders group that was located predominantly in left temporal and parietal regions (i.e. the superior temporal sulcus, inferior temporal, postcentral/superior parietal and supramarginal gyri). These findings remained largely unchanged after controlling for intelligence quotient and after accounting for psychotropic medication usage and comorbid psychopathology. Furthermore, a significant age × diagnosis interaction was found in the left fusiform/inferior temporal cortex: participants with autism spectrum disorders had thinner cortex in this region with increasing age to a greater degree than did typically developing participants. Follow-up within group comparisons revealed significant age-related thinning in the autism spectrum disorders group but not in the typically developing group. Both thinner temporal and parietal cortices during adolescence and young adulthood and discrepantly accelerated age-related cortical thinning in autism spectrum disorders suggest that a second period of abnormal cortical growth (i.e. greater thinning) may be characteristic of these disorders.
"Sepsis in infants was fi rst linked to white matter damage in the 1970s (Leviton and Gilles, 1973), and there is now a strong literature linking perinatal infection to cerebral palsy (see Garnier et al., 2003; Huleihel et al., 2004 for review). Beyond these major developmental impairments, one of the most common consequences of perinatal infection/infl ammation generally is cognitive dysfunction, including learning, memory, and attention disorders (Bauman et al., 1997). E. coli infections in particular in premature infants are associated with signifi cant neurodevelopmental delays, which occur regardless of infection location (e.g., brain, blood, or intestines; Stoll et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: The immune system is well characterized for its critical role in host defense. Far beyond this limited role however, there is mounting evidence for the vital role the immune system plays within the brain, in both normal, "homeostatic" processes (e.g., sleep, metabolism, memory), as well as in pathology, when the dysregulation of immune molecules may occur. This recognition is especially critical in the area of brain development. Microglia and astrocytes, the primary immunocompetent cells of the CNS, are involved in every major aspect of brain development and function, including synaptogenesis, apoptosis, and angiogenesis. Cytokines such as tumor necrosis factor (TNF)alpha, interleukin [IL]-1beta, and IL-6 are produced by glia within the CNS, and are implicated in synaptic formation and scaling, long-term potentiation, and neurogenesis. Importantly, cytokines are involved in both injury and repair, and the conditions underlying these distinct outcomes are under intense investigation and debate. Evidence from both animal and human studies implicates the immune system in a number of disorders with known or suspected developmental origins, including schizophrenia, anxiety/depression, and cognitive dysfunction. We review the evidence that infection during the perinatal period of life acts as a vulnerability factor for later-life alterations in cytokine production, and marked changes in cognitive and affective behaviors throughout the remainder of the lifespan. We also discuss the hypothesis that long-term changes in brain glial cell function underlie this vulnerability.
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