A variant of autism spectrum disorder (ASD) known as Asperger syndrome (AS) is characterized by severe issues with interpersonal, verbal, and nonverbal communication as well as restricted and repetitive patterns of behavior and activities. Although there is no known cause for ASD, various genetic as well as non-genetic risk factors that may act either alone or in combination to induce ASD have been identified. The occurrence of ASD has been increasing worldwide. Co-occurring neuropsychological diseases are frequently present as well. The premise for diagnosis is the observation of abnormal conduct, with diagnostic criteria emphasizing limitations in social interaction and communication as well as constrained, repetitive behavioral patterns, activities, or hobbies. The degree of the illness and the presence of intellectual impairment have a significant impact on the prognosis. Like autism, Asperger's can neither be prevented nor treated. There is no specific medical therapy that can effectively cure all of the symptoms of autism. However, medications may be used as adjuvant therapy for maladaptive behaviors and co-occurring mental problems. The treatment aims to reduce core impairments, increase functional ability, and reduce harmful behaviors that could limit functional skills. It is crucial to provide proper care, establish supportive networks for individuals who are affected and their families, and use effective therapies to enhance functioning and results.

Changes in the brain's default mode network (DMN) in the resting state are closely related to autism spectrum disorder (ASD). Module segmentation can effectively elucidate the neural mechanism of ASD and explore intra- and inter-network connections by means of the participation coefficient (PC). We used that resting-state fMRI data from 269 ASD patients and 340 healthy controls (HCs) in the current study. From the results, ASD subjects showed a significantly higher PC of the DMN than HC subjects. This difference was related to lower intra-module connections within the DMN and higher inter-network connections between the DMN and other networks. When the subjects were split into age groups, the results were verified in the 7-12- and 12-18-year-old age groups but not in the young adult group (18-25 years). When the subjects were divided according to different subtypes of ASD, the results were also observed in the classic autism and pervasive developmental disorder groups, but not in the Asperger disorder group. In conclusions, less developed network segregation in the DMN could be a valid biomarker for ASD. This provides network scientists with new insights into the intermodular connectivity configurations of complex networks from different dimensions in a systematic and comprehensive manner.

To make decisions in mental health care, service users, clinicians, and administrators need to make sense of research findings. Unfortunately, study results are often presented as raw questionnaire scores at different time points and regression coefficients, which are difficult to interpret with regards to their clinical meaning. Other commonly reported treatment outcome indicators in clinical trials or meta-analyses do not convey whether a given change score would make a noticeable difference to service users. There is an urgent need to improve the interpretability and relevance of outcome indicators in youth mental health (aged 12-24 years), in which shared decision making and person-centred care are cornerstones of an ongoing global transformation of care. In this Personal View, we make a case for considering minimally important change (MIC) as a meaningful, accessible, and user-centred outcome indicator. We discuss what the MIC represents, how it is calculated, and how it can be implemented in dialogues between clinician and researcher, and between youth and clinician. We outline how use of the MIC could enhance reporting in clinical trials, meta-analyses, clinical practice guidelines, and measurement-based care. Finally, we identify current methodological challenges around estimating the MIC and areas for future research. Efforts to select outcome domains and valid measurement instruments that resonate with youth, families, and clinicians have increased in the past 5 years. In this context, now is the time to define demarcations of changes in outcome scores that are clinically relevant, and meaningful to youth and families. Through the use of MIC, youth-centred outcome measurement, analysis, and reporting would support youth-centred therapeutic decision making.

Autism spectrum disorders (ASDs) are a group of neurodevelopmental pathologies characterized by social and communication deficits, for which treatments are limited. Cell therapies, including intrathecal (IT) administration of bone marrow (BM) mononuclear cells (BM-MNC), improves symptoms in patients with ASD. Twenty-four patients diagnosed with ASD, according to the Diagnostic and Statistical Manual of Mental Disorders Text Revision Fourth Edition (DSM-IV-TR) criteria, were autologously treated with IT BM-MNC, and the clinical effect was evaluated using the Childhood Autism Rating Scale (CARS) on Days 30 (n=24) and 180 (n=14) post-treatment. IT BM-MNC improved clinical outcomes by Day 30 (p=0.0039), and those benefits remained and were further accentuated by Day 180 post-treatment (n=14; p=<0.0001). Clinical benefit at Days 30 (p=0.001; r= -0.51) and 180 (p=0.01; r= -0.60) posttreatment positively correlated with the enrichment of a putative BM stem cell population expressing the cluster of differentiation 133+ (CD133+) surface marker.

Self-report measures are central in capturing young people's perspectives on mental health concerns and treatment outcomes. For children and adolescents to complete such measures meaningfully and independently, the reading difficulty must match their reading ability. Prior research suggests a frequent mismatch for mental health symptom measures. Similar analyses are lacking for measures of Quality of Life (QoL). We analysed the readability of 13 commonly used QoL self-report measures for children and adolescents aged 6 to 18 years by computing five readability formulas and a mean reading age across formulas. Across measures, the mean reading age for item sets was 10.7 years (SD = 1.2). For almost two-thirds of the questionnaires, the required reading age exceeded the minimum age of the target group by at least one year, with an average discrepancy of 3.0 years (SD = 1.2). Questionnaires with matching reading ages primarily targeted adolescents. Our study suggests a frequent mismatch between the reading difficulty of QoL self-report measures for pre-adolescent children and this group's expected reading ability. Such discrepancies risk undermining the validity of measurement, especially where children also have learning or attention difficulties. Readability should be critically considered in measure development, as one aspect of the content validity of self-report measures for youth.

One of the great challenges in psychiatry is finding reliable biomarkers that may allow for more accurate diagnosis and treatment of patients. Neural variability received increasing attention in recent years as a potential biomarker. In the present explorative study we investigated temporal variability in visually evoked EEG activity in a cohort of 16 adult participants with Asperger Syndrome (AS) and 19 neurotypical (NT) controls. Participants performed a visual oddball task using fine and coarse checkerboard stimuli. We investigated various measures of neural variability and found effects on multiple time scales. (1) As opposed to the previous studies, we found reduced inter-trial variability in the AS group compared to NT. (2) This effect builds up over the entire course of a 5-min experiment and (3) seems to be based on smaller variability of neural background activity in AS compared to NTs. The here reported variability effects come with considerably large effect sizes, making them promising candidates for potentially reliable biomarkers in psychiatric diagnostics. The observed pattern of universality across different time scales and stimulation conditions indicates trait-like effects. Further research with a new and larger set of participants are thus needed to verify or falsify our findings.

The origin of moral agency is a much-debated issue. While rationalists or Kantians have argued that moral agency is rooted in reason, sentimentalists or Humeans have ascribed its origin to empathic feelings. This debate between rationalists and sentimentalists still stands with respect to persons with mental disorders, such as individuals diagnosed with mild forms of Autism Spectrum Disorder (ASD), without intellectual impairment. Individuals with ASD are typically regarded as moral agents, however their ability for empathy remains debated. The goal of this paper is to investigate the mechanisms of moral actions in people with ASD, by finding arguments for the origin of their moral actions, supporting either the sentimentalist or the rationalist view of the dispute. We propose to revisit the debate using Interpretative Phenomenological Analysis to study the autobiographies of individuals with High-Functioning Autism (HFA) and Asperger Syndrome (AS). While conducting the systematic analysis of 10 autobiographies, we re-examined both the rationalist and the sentimentalist positions, considering the links between empathic feelings and moral agency. The investigation of the temporal dimensions of emotional experiences, an aspect overlooked by previous research, indicated that individuals with ASD empathize with others, but in different ways as compared to neurotypicals. A relationship between emotional experience and the type of moral agency exhibited by individuals with forms of ASD was established. As a consequence, our analyses support the sentimentalist stance on moral action.

There is very little knowledge regarding autistic adult services, practices, and delivery. The study objective was to improve understanding of current services and practices for autistic adults and opportunities for improvement as part of the Autism Spectrum Disorder in the European Union (ASDEU) project. Separate survey versions were created for autistic adults, carers of autistic adults, and professionals in adult services. 2,009 persons responded to the survey and 1,085 (54%) of them completed at least one of the services sections: 469 autistic adults (65% female; 55% <35 years old), 441 carers of autistic adults (27% female; 6% <35 years old), 175 professionals in adult services (76% female; 67% in non-medical services). Top choices by autistic adults, carers or professionals for services best suiting their current needs were: residential services: "help in own home" (adults, carers of high independent adults, professionals), "fulltime residential facility" (carers of low independent adults); employment services: "job mentors" (adults, carers of high independent adults, professionals), "Sheltered employment" (carers of low independent adults); education services: "support in regular education setting" (all groups); financial services: financial support in lieu of employment ("Supplementary income for persons unable to have full employment" for adults, "full pension" for carers of low independent adults) or to supplement employment earnings for carers of high independent adults and professionals; social services: "behavior training" (adults) and "life skills training" (carers and professionals). Waiting times for specific services were generally < 1 month or 1-3 months, except for residential services which could be up to 6 months; most professionals were uninformed of waiting times (>50% responded "don't know"). Five of seven residential services features recommended for autistic adults were experienced by <50% of adults. The knowledge of good local services models that work well for autistic adults was generally low across all services areas. The variation in services experiences and perceptions reported by autistic adults, carers, or professionals underscore the need to query all groups for a complete picture of community services availability and needs. The results showed areas for potential improvement in autistic adult services delivery in the EU to achieve recommended standards.

Next-generation sequencing techniques have accelerated the discovery of rare mutations responsible for autism spectrum disorder (ASD) in genes involved in a large number of physiological processes, including the control of gene expression, chromatin remodeling, signaling pathways, synaptic scaffolding, neurotransmitter receptors, and lipid metabolism. Genetic diagnosis provides subjects with an explanation of the cause of their disorder. However, it does not, or at least does not yet, shed light on the psychopathological phenomena specific to the individual. It could be hypothesized that each physiological impact of a mutation corresponds to a specific psychopathological phenomenon of ASD, i.e., "a psychopathological natural kind". We discuss here the difficulties identifying this specificity of underlying psychopathology in individuals with ASD due to a rare mutation with a major effect. A comparison of Newson's pathological demand avoidance and Wing's Asperger's syndrome with Asperger's autistic psychopathy highlights different ways of approaching psychopathological descriptions and diagnosis, by focusing on either common or unusual features. Such a comparison calls into question the principles of clinical research recommended by Falret for characterizing "disease individuality" of ASD due to a rare mutation.

Asperger syndrome (AS) was first described by Hans Asperger in 1944, as the behavioral characterization of individuals who have difficulties in communication and social interaction.[1] Since then, AS has always been a topic of significant interest and debate. Although AS was introduced as a discrete diagnostic category in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-4, 1994), almost 20 years later, its diagnostic label was removed in the Diagnostic and Statistical Manual of Mental Disorders (DSM–5), and it was encompassed in a more general category of autism spectrum disorders (ASD).[2] According to the DSM-5, there are varying degrees of ASD that are categorized based on the severity of symptoms and the required levels of support, and what was formerly called Asperger syndrome shall now be regarded as ASD.[3] Autism spectrum disorders (ASD) include a group of neurodevelopmental abnormalities with broadly varying degrees and manifestations, usually begin in early childhood, and characterized by problems in social communication and interaction, along with behavioral problems such as restricted interests and repetitive behaviors.[4][5] DSM-5 changes on ASD classification led to some controversy about the loss of the unique Asperger identity,[6] and literature continue to debate about AS and its formulation within ASD.[7] Due to Asperger syndrome's extensive history, rich semiology, and relatively characteristic clinical presentations, specialists continue to use this diagnosis as a subtype of ASD with no language delay and a normal or superior IQ.[6] In this topic review, we will describe the essential aspects of autism spectrum disorder and Asperger syndrome. For greater transparency, we refer to (1) Asperger syndrome (AS) as a subpopulation of pervasive developmental disorders (PDD) according to DSM-IV-TR, (2) ASD according to DSM-5, and (3) Autism spectrum disorder of an Asperger syndrome type (ASD-AS) as a subpopulation that is included in the DSM-5 as ASD of level 1 severity without intellectual impairment. Historical Perspective In 1944, and about a year after Leo Kanner described infantile autism, Hans Asperger introduced autistic psychopathy in the form of a case report. In 1980, the American Psychiatric Association (APA) recognized autism as a distinct category in the DSM-3 and introduced it as infantile autism. In 1981, Wing L. restarted Asperger researches and renamed autistic psychopathy as Asperger syndrome. A few years later and in 1989, the first diagnostic criteria for AS was proposed,[7] and the 10th Revision of the International Classification of Diseases (ICD-10) was the first major classification system that recognized AS (1993). Finally, in 1994, AS was introduced in DSM-4 as a specific entity along with autistic disorder, within pervasive developmental disorders (PDD). While during this period, researches were focused on the development of measures with the ability to diagnose AS and differentiate it from high functioning autism (HFA), the DSM-5 removed the diagnostic category of AS in 2013.[5] The World Health Organization (WHO) also followed a similar approach in ICD-11, which will come into effect in 2022.[2] DSM Classification The systematic description of psychiatric disorders is quite complicated, particularly in child and adolescent psychiatry. Asperger syndrome was included in the DSM-IV-TR in the large family of pervasive developmental disorders (PDD). PDD had five subtypes: Autistic disorder. Asperger syndrome. Childhood disintegrative disorder. Pervasive developmental disorder-not otherwise specified (PDD-NOS). Rett syndrome. Symptoms and clinical specifiers for autistic disorder of PDD were described to fall into three broad categories in DSM IV-TR: (1) social interaction, (2) communication, and (3) restricted, repetitive behavior.[8] The diagnosis of AS required:[7]: At least two symptoms of social interaction impairment and at least one each from symptoms of communication and restricted, repetitive behavior (RRB). Delays or abnormal functioning in at least one of the areas of (1) social interaction, (2) language as used in social communication, or (2) symbolic or imaginative play with onset prior to age 3 years. Diagnostic criteria for autistic disorder (or another specific PDD) should not be met (otherwise, the AS diagnosis is excluded, and autistic disorder diagnosis should have precedence). AS contrasted from autistic disorder in:[9]: Absence of diagnostic criteria in the communication domain. Absence of a requirement for onset before age 3. Addition of criteria specifying the absence of a language delay. Addition of criteria specifying the absence of a deficit in cognitive development. This classification suggested a differential diagnosis between AS and the type of Autistic disorder associated with normal cognitive functioning, also known as high functioning autism (HFA). As a result, it sparked substantial debate over uncertainty in defining AS criteria and the clinical overlap between AS and HFA, which has appeared in literature with contradictory results. Although there has been a considerable number of researches showing some fine differences between the two disorders, most studies have emphasized the meaningful similarities between AS and HFA.  Ultimately, the DSM-5 removed PDD and its categorization and merged four of its subtypes into one unifying category with the concept of a continuum named autistic spectrum disorders (ASD). This major alteration was mostly due to the assumption that PDD subgroups cannot be differentiated from one another certainly and reliably.[7] These changes include the following:[2][8] Another major alteration was the inclusion of social communication and social interaction related deficits in one criterion and exclusion of deficit specifically related to spoken language. Elimination of PDD and its subtypes. Creation of a new diagnostic category called autistic spectrum disorders (ASD), encompassing autistic disorder, Asperger syndrome, childhood disintegrative disorder, and PDD-NOS. Addition of three levels of severity, and clinical specifiers about the presence of cognitive and language impairment, to better characterize the diagnosis. Changing from previous PDD 3-domain criteria to ASD 2-domain criteria, composed of impaired social communication/interaction and restricted, repetitive behavior, interest, and activities (merging domains of social interaction and communication). Addition of sensory symptoms in the RRB component of diagnostic criteria. Changing the specification of the age of onset from age 3 to "early childhood.". Creation of a new diagnostic category called "social communication disorder" (SCD) to include individuals who have difficulties in social communication/interaction but do not meet RRB criteria found in ASD. Removal of Rett syndrome from the classification, on the basis of recent genetic data. Controversy over the New Classification of ASD The new classification of ASDs has been criticized in the literature in different ways. Some authors have suggested that the new classification will narrow the criteria for ASD; thus, some patients may no longer meet the criteria for ASD, in particular, cognitively able individuals and individuals diagnosed with AS and PDD-NOS. In short, the argument is although this reduced sensitivity is associated with higher specificity, it has the potential to exert negative effects on the service eligibility, as well as the ability of researchers to integrate information and data from researches conducted under these criteria.[9][6] Other authors claim that the elimination of the specific diagnostic category for Asperger syndrome will increase stigma towards individuals previously diagnosed with AS, based on the assumption that autism-phobic societies perceive autism as a significant disability, whereas AS is associated with the more positive stereotypes.[10][2] In addition, previous research has demonstrated the association of autism with disability and dysfunction, and the association of AS with positive features. Thus, the new inclusion of AS in the category of ASD may have a negative effect on the identity of the individuals who have adopted this label as an identity. However, the literature on the potential impact of the DSM-5 changes on individuals previously diagnosed with AS is limited, and the results can be categorized into those who are supportive, those who are opposed, and those who express mixed feelings concerning the changes.[2]

Over the past few decades, neuroimaging has become a ubiquitous tool in basic research and clinical studies of the human brain. However, no reference standards currently exist to quantify individual differences in neuroimaging metrics over time, in contrast to growth charts for anthropometric traits such as height and weight1. Here we assemble an interactive open resource to benchmark brain morphology derived from any current or future sample of MRI data (http://www.brainchart.io/). With the goal of basing these reference charts on the largest and most inclusive dataset available, acknowledging limitations due to known biases of MRI studies relative to the diversity of the global population, we aggregated 123,984 MRI scans, across more than 100 primary studies, from 101,457 human participants between 115 days post-conception to 100 years of age. MRI metrics were quantified by centile scores, relative to non-linear trajectories2 of brain structural changes, and rates of change, over the lifespan. Brain charts identified previously unreported neurodevelopmental milestones3, showed high stability of individuals across longitudinal assessments, and demonstrated robustness to technical and methodological differences between primary studies. Centile scores showed increased heritability compared with non-centiled MRI phenotypes, and provided a standardized measure of atypical brain structure that revealed patterns of neuroanatomical variation across neurological and psychiatric disorders. In summary, brain charts are an essential step towards robust quantification of individual variation benchmarked to normative trajectories in multiple, commonly used neuroimaging phenotypes.

Asperger syndrome (AS) is a chronic neurodevelopmental disorder. Although all of the clinically diagnosed cases display normal intelligence and speech functions, barriers in social interaction and communication seriously affect mental health and psychological function. In addition to traditional psychological/behavioral training and symptomatic medication, in-depth studies of intestinal microbiota and mental health have indicated that probiotics (e.g., Lactobacillus rhamnosus) can effectively reduce the occurrence of AS. Fecal microbiota transplantation (FMT) is a type of biological therapy that involves the transplant of intestinal microbiota from healthy donors into the patient's gastrointestinal tract to improve the gut microenvironment. In this case report, we describe the first case of adult AS treated with FMT. The patient suffered from diarrhea-predominant irritable bowel syndrome for 6 years with symptoms of diarrhea and abdominal pain. After three rounds of FMT, the diarrhea and abdominal pain were significantly improved. Moreover, the symptoms of AS were also significantly ameliorated. We found that FMT changed the structure of the intestinal microbiota as well as the patient's serum metabolites, and these changes were consistent with the patient's symptoms. The metabolites may affect signaling pathways, as revealed by Kyoto Encyclopedia of Genes and Genomes enrichment analysis. The changes in microbial metabolites following FMT may affect other regions (e.g., the nervous system) via the circulatory system, such that the bacteria-gut-blood-brain axis may be the means through which FMT mitigates AS.

Findings of the fatty acid status of people with autism spectrum disorders have been incongruent perhaps because of the diversity of the condition. A cross-sectional design study was used to investigated fatty acid levels and relationships between fatty acids, and cognition and behaviour in a homogenous group of children with autism spectrum disorder. Children with Asperger's syndrome (AS) /high functioning autism (n = 44) and healthy siblings (n = 17) were recruited from the Diagnostic and Therapeutic Centre for Children with Autism, Warsaw, Poland. In the AS group, plasma phosphatidylcholine 22:5n3 correlated positively with verbal (r = 0.357, p = 0.019) and full scale (r = 0.402, p = 0.008) IQs, red blood cell phosphatidylcholine 22:5n3 with verbal (r = 0.308, p = 0.044), performance (r = 0.304, p = 0.047) and full scale (r = 0.388, p = 0.011) IQs and red blood cell phosphatidylethanolamine 22:5n3 with verbal (r = 0.390, p = 0.010) and full scale (r = 0.370, p = 0.016) IQs. Whilst, plasma phosphatidycholine 20:5n3 (r = -0.395, p = 0.009), 22:6n3 (r = -0.402, p = 0.007) and total n3 fatty acids (r = -425, p = 0.005), red blood cell phosphatidlycholine 20:5n3 (r = -0.321, p = 0.036) and red blood cell phosphatidylethanolamine 20:5n3 (r = -0.317, p = 0.038), 22:6n3 (r = -0.297, p = 0.05) and total n3 fatty acids (r = -0.306, p = 0.046) correlated inversly with ADHD index. Similarly, inattention was negatively related with plasma phosphatidylcholine 22:6n3 (r = -0.335, p = 0.028), and total n3 fatty acids (r = -0.340, p = 0.026), oppositional with plasma phosphatidylcholine 18:3n3 (r = -0.333, p = 0.029), 20:5n3 (r = -0.365, p = 0.016), total n3 fatty acids (r = -0.293, p < 0.05), red blood cell phosphatidylcholine 18:3n3 (r = -0.337, p = 0.027) and red blood cell ethanolamine 18:3n3 (r = - 0.333, p = 0.029), 20:5n3 (r = -0.328, p = 0.032), 22:6n3 (r = 0.362, p = 0.017) and total n-3 fatty acids (r = -0.298, p < 0.05) and hyperactivity with plasma phosphatidylcholine 22:6n3 (r = -0.320, p = 0.039). In contrast, there were inverse correlations between red blood cell phosphatidylcholine 18:2n6 and performance (r = -0.358, p = 0.019) and full scale (r = -0.320, p = 0.039) IQs, and direct correlations between red blood cell phosphatidylcholine 22:4n6 (r = 0.339, p = 0.026) and 22:5n6 (r = 0.298, p < 0.05) and ADHD index, between red blood cell phosphatidylcholine 22:4n6 (r = 0.308, p = 0.044) and inattention, between plasma phosphatidylcholine 22:4n6 (r = 0.341, p = 0.025), red blood cell phosphatidylcholine 20:4n6 (r = 0.314, p = 0.041) and total n6 fatty acids (r = 0.336, p = 0.028) and oppositional and plasma phosphatidylcholine 20:3n6 (r = 0.362, p = 0.018) and red blood cell phosphatidylcholine 20:3n6 (r = 0.401, p = 0.009) and hyperactivity. The findings of the ethnically homogenous children with Asperger's syndrome/high functioning autism study revealed positive associations between 22:5n3 and cognition, and negative relationships between 20:5n3 and 22:6n3 and behavioural problem. In contrast, cognitive ability and behavioural problems were negatively and positively associated with n6 fatty acids. Further investigation is required to establish whether there a cause and effect relationship. Regardless, it would be prudent to ensure that children with the conditions have optimum n3 PUFA intake.

The current version of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM-V) does not consider Asperger syndrome a diagnostic category. This study was undertaken to see if there is evidence that this diagnosis should be reinstated. An online survey was conducted to examine symptoms and behaviors associated with the current diagnostic criteria of autism spectrum disorders (ASD) (DSM-V), and those associated with Asperger syndrome based on the previous version (DSM-IV-TR). The study also examined other characteristics historically associated with autism, as well as impairments often reported in infancy/young childhood and medical comorbidities frequently associated with autism. The sample included 251 individuals who had received a diagnosis of Asperger syndrome and 1888 who were diagnosed with autism or ASD. Numerous similarities and differences were found between the two groups. The findings are discussed in relation to reestablishing Asperger syndrome as a valid diagnostic category as well as a subtype of ASD.

Sleep spindles are an element of the sleep microstructure observed on the EEG during the NREM sleep phase. Sleep spindles are associated to sleep stability functions as well as memory consolidation and optimization of different cognitive processes. On the other hand, Asperger's syndrome (AS) is a generalized developmental disorder in which cognitive and sleep disturbances have been described. In this study we analyzed different characteristics of sleep spindles in a group of children with AS and compared them with sleep spindles of a group of children with typical development paired by age; both groups ranged from 6 to 12 years of age and were all male. We observed a statistically significant decrease in sleep spindles intrinsic frequency in different brain regions in the AS group in relation to the typical development group. This finding could be due to immaturity in brain regions related to the integration of sleep spindles; and this immaturity could be related with cognitive aspects in these patients.

Because of a painful right-sided coxarthrosis a 57-year-old female patient underwent a cementless total arthroplasty under general anesthesia. Except for Asperger's syndrome and an occlusion of a vein in her left eye she stated no other diseases or complaints, especially no cardiac problems. Postoperatively she developed neurological symptoms of left-sided hemiparesis and hemihypesthesia. A cranial computer tomography was performed and a right-sided infarction of the thalamic region was found. A patent foramen ovale (PFO) and atrial septal aneurysm were detected 5 days later. The incidence of a PFO is given as 25% of the population. A paradoxical air embolism in the presence of a PFO is a feared complication in neurosurgical interventions in a semi-sitting or sitting position. Corpuscular emboli, such as bone, cement, fat or wound debris may be the reason for paradoxical embolisms in combination especially with partial or total hip replacement. The kind of embolism in the case described could not be clarified. Deep vein thrombosis or cardiac arrhythmia could be excluded. Therefore, it can be considered most likely that the operation site was the source of the embolism. The trigger for a paradoxical embolism is a reversal of the pressure difference between the right and left atria: normally the left atrial pressure exceeds the right atrial pressure by ca. 2-4 mm Hg, resulting possibly in a small clinically irrelevant left-to-right shunt. If the pulmonary arterial circulation is compromised and pulmonary vascular resistance increases, the pressure gradient between the left and right atria reverses and a right-to-left shunt can occur causing a paradoxical embolism. Positive end-expiratory pressure (PEEP) ventilation during anesthesia could be an important reason for a shunt reversal between the right and left atria and therefore favoring a paradoxical embolism but the pathophysiological role of PEEP has not yet been finally clarified.