1. Hollander E, Wang AT, Braun A, Marsh L. {{Neurological considerations: autism and Parkinson’s disease}}. {Psychiatry Res};2009 (Nov 30);170(1):43-51.
Within the spectrum of disorders that manifest obsessive-compulsive (OC) features lies a sub-cluster of neurological conditions. Autism and Parkinson’s disease (PD) are examples of two such neurological disorders that seem quite dissimilar on the surface. Yet, both conditions can include repetitive behaviors of a compulsive-impulsive nature. Furthermore, while autism and PD differ in other associated symptom domains that shape the course of each disorder, both disorders share some phenomenology in the core domain of repetitive behaviors and involve basal ganglia and frontal lobe dysfunction, similar to OC disorder (OCD). Accordingly, examination of the similarities and differences between autism and PD may provide insight into the pathophysiology and treatment of OC spectrum disorders. The current review focuses on the phenomenology, comorbidity, course of illness, family history, brain circuitry, and treatment of autism and PD, as they relate to OCD and OC spectrum disturbances.
2. Magalhaes ES, Pinto-Mariz F, Bastos-Pinto S, Pontes AT, Prado EA, deAzevedo LC. {{Immune allergic response in Asperger syndrome}}. {J Neuroimmunol};2009 (Nov 30);216(1-2):108-112.
Asperger’s syndrome is a subgroup of autism characterized by social deficits without language delay, and high cognitive performance. The biological nature of autism is still unknown but there are controversial evidence associating an immune imbalance and autism. Clinical findings, including atopic family history, serum IgE levels as well as cutaneous tests showed that incidence of atopy was higher in the Asperger group compared to the healthy controls. These findings suggest that atopy is frequent in this subgroup of autism implying that allergic inflammation might be an important feature in Asperger syndrome.
3. Onore C, Enstrom A, Krakowiak P, Hertz-Picciotto I, Hansen R, Van de Water J, Ashwood P. {{Decreased cellular IL-23 but not IL-17 production in children with autism spectrum disorders}}. {J Neuroimmunol};2009 (Nov 30);216(1-2):126-129.
A potential role for T(H)17 cells has been suggested in a number of conditions including neurodevelopmental disorders such as autism spectrum disorders (ASD). In the current study, we investigated cellular release of IL-17 and IL-23 following an in-vitro immunological challenge of peripheral blood mononuclear cells (PBMC) from children with ASD compared to age-matched typically developing controls. Following stimulation, the concentration of IL-23, but not IL-17, was significantly reduced (p=0.021) in ASD compared to controls. Decreased cellular IL-23 production in ASD warrants further research to determine its role on the generation and survival of T(H)17 cells, a cell subset important in neuroinflammatory conditions that may include ASD.
4. Wilson LB, Tregellas JR, Hagerman RJ, Rogers SJ, Rojas DC. {{A voxel-based morphometry comparison of regional gray matter between fragile X syndrome and autism}}. {Psychiatry Res};2009 (Nov 30);174(2):138-145.
The phenotypic association between fragile X syndrome (FXS) and autism is well established, but no studies have directly compared whole-brain anatomy between the two disorders. We performed voxel-based morphometry analyses of magnetic resonance imaging (MRI) scans on 10 individuals with FXS, 10 individuals with autism, and 10 healthy comparison subjects to identify volumetric changes in each disorder. Regional gray matter volumes within frontal, parietal, temporal, and cingulate gyri, as well as in the caudate nuclei and cerebellum, were larger in the FXS group relative to the autism group. In addition, volume increases in FXS were observed in frontal gyri and caudate nuclei compared to controls. The autism group exhibited volume increases in frontal and temporal gyri relative to the FXS group, and no volume increases relative to controls. Volumetric deficits relative to controls were observed in regions of the cerebellum for both groups, with additional deficits in parietal and temporal gyri for the FXS group. Our caudate nuclei and frontal gyri results may implicate dysfunction of frontostriatal circuitry in FXS. Cerebellar deficits suggest atypical development of the cerebellum contributing to the phenotype of both disorders, but further imply that unique cerebellar regions contribute to the phenotype of each disorder.
