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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autistic children were compared with control children on tasks in which retention was tested by different methods. In three tests of recall, using named pictures, written words and spoken words as test stimuli, autistic children were impaired in comparison with age-matched normal children and with controls matched for verbal ability. In one test of forced-choice recognition of pictures, autistic children were impaired in comparison with ability-matched controls. In three tests of cued recall, using named pictures, written words and spoken words as test stimuli, and acoustic, graphemic and semantic cues, autistic children were not impaired in comparison with normal age-matched controls. In one test of paired-associate learning using non-related word pairs as test stimuli autistic children were not impaired in comparison with normal age-matched controls. These experimental paradigms were similar to some that have been used to investigate the amnesic syndrome in man. Thus findings on paired-associate learning differ in autistic and amnesic subjects, but findings on recall, recognition and cued recall are comparable. A possible parallel between autism and amnesia is discussed.
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PMID:Memory deficits in early infantile autism: some similarities to the amnesic syndrome. 126 53

Medial temporal lobe amnesic disorder is characterized by an impairment in explicit memory (e.g., remembering a shopping list) and intact implicit memory (e.g., a woman seems familiar although you cannot remember having met her before). This study examined whether children with high-functioning autism have this same dissociation between explicit and implicit memory abilities. Children with autism and normal development participated in three memory tasks: one implicit task (perceptual identification) and two explicit tasks (recognition and recall). Children with autism showed intact implicit and explicit memory abilities. However, they did not show the typical pattern of recalling more items from both the beginning and end of a list and instead only recalled items from the end of the list. These results do not support the theory that high-functioning autism is a type of medial temporal lobe amnesia. However, these findings suggest that persons with autism use different organizational strategies during encoding or retrieval of items from memory.
J Autism Dev Disord 2000 Feb
PMID:Implicit and explicit memory in autism: is autism an amnesic disorder? 1081 16

Much research about memory in autism concerns the hypothesis that autism is similar to adult-onset amnesia. Initial support for the hypothesis came from post-mortem studies of individuals with autism showing abnormalities in the hippocampus and related brain structures, as well as behavioral studies finding contrasts between intact cued recall and impaired free recall and recognition in autism. The hypothesis was later brought into question by the finding of intact performance in individuals with autism on explicit memory tasks typically impaired in adult-onset amnesia. The present paper proposes a possible reconciliation of these contradictory findings, suggesting that there is selective damage to the limbic-prefrontal episodic memory system, sparing the limbic-only perceptual representation system, and the semantic memory system. This view is consistent with other evidence for early selective damage to other systems involving cooperation between the limbic system and the medial prefrontal cortex in autism.
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PMID:Memory in autism: review and synthesis. 1458 70

Although cognitive psychology has learned much from the study of patients with neuropsychological impairments, social and personality psychologists have been slow to do the same. In this article we argue that the domain of clinical neuropsychology holds considerable untapped potential for formulating and testing models within social and personality; psychology and describe some of the ways in which questions of interest to social and personality psychologists can be addressed with neuropsychological data. Examples are drawn from a variety of neuropsychological syndromes, including amnesia, autism, anosognosia, commissurotomy, frontal lobe damage, and prosopagnosia. We conclude that consideration of the personal and social lives of patients with neuropsychological impairments ultimately will lead to a richer understanding of the person, one that bridges the gap between social and cognitive levels of analysis.
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PMID:On bridging the gap between social-personality psychology and neuropsychology. 1564 31

We start by assuming that the self is implemented in the brain as a functional unit, with a definite set of properties. We deduce the fundamental properties of the self from an analysis of neurological disorders and from introspection. We formulate a functionalist concept of the self based on these properties reduced to constraints. We use the formalism of schemas in our functionalist analysis, i.e. a symbolic level description of brain dynamics. We then reformulate the functionalist model at a connectionist level and address the emergent "context shifting" problem. We suggest how the model might be mapped onto the functional neuroanatomy of the brain, and how it could be used to give an account of a range of neurological disorders, including hippocampal amnesia, various forms of schizophrenia, multiple personality, autism, PTSD, hemineglect, and reversible anosognosia. Finally, we briefly discuss future perspectives and possible applications of computer implementations of the model.
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PMID:Fundamental principles and mechanisms of the conscious self. 1620 31

Bipedal locomotion and fine motility of hand and larynx of humans introduced musculoskeletal adaptations, new pyramidal, corticostriatal, corticobulbar, nigrostriatal, and cerebellar pathways and expansions of prefrontal, cingular, parieto-temporal and occipital cortices with derived new brain capabilities. All selectively degenerate in aged homo sapiens following 16 syndromic presentations: (1) Parkinsonism: nigrostriatal control for fast automatic movements of hand, larynx, bipedal posture and gait ("simian gait and hand"). (2) Frontal (highest level) gait disorders (lower body parkinsonism, gait apraxia, retropulsion): prefrontostriatal executive control of bipedal locomotion. (3) ataxia: new synergistic coordination of bipedal gait and fine motility. (4) Dyskinesias (chorea, dystonia, tremor...): intrusions of simian basal ganglia motor subroutines. (5) motoneuron diseases: new proximo-distal and bulbar motoneurones, preserving older ones (oculomotor, abdominal...). (6) Archaic reflexes: prefrontal disinhibition of old mother/tree-climbing-oriented reflexes (sucking, grasping, Babinski/triple retraction, gegenhalten), group alarms (laughter, crying, yawning, grunting...) or grooming (tremor=scratching). (7) Dysautonomia: contextual regulation (orthostatism...). (8) REM sleep disorders of new cortical functions. (9) Corticobasal syndrome: melokinetic control of hand prehension-manipulation and language (retrocession to simian patterns). (10) Frontal/temporal lobe degeneration: medial-orbitofrontal behavioural variant: self monitoring of internal needs and social context: apathy, loss of personal hygiene, stereotypia, disinhibition, loss of concern for consequences of acts, social rules, danger and empathy; dorsolateral executive variant: inadequacy to the context of action (goal, environmental changes...); progressive non-fluent aphasia: executive and praxic processing of speech; temporal variant: abstract concepts for speech, gestures and vision (semantic dementia, progressive nonfluent aphasia) (11) Temporomesial-limbic-paralimbic-associative cortical dementias (Alzheimer's disease, Lewy body, progressive amnesia): processing of explicit cognition: amnesic syndrome, processing of hand, larynx and eye: disorientation, ideomotor apraxia, agnosia, visuospatial processing, transcortical aphasia. (12) Focal posterior atrophy (Benson, progressive apraxia): visuomotor processing of what and where. (13) Macular degeneration: retinal "spot" for explicit symbols. (14) "Psychiatric syndromes": metacognition, self monitoring and regulation of hierarchical processing of metacognition: hallucinations, delusions, magic and mystic logic, delusions, confabulations; drive: impulsivity, obsessive-compulsive disorders, mental automatisms; social interactions: theory of mind, autism, Asperger. (15) Mood disorders: control on emotions: anxio-depressive and bipolar disorders, moria, emotional lability. (16) Musculoskeletal: inclusion body myositis: muscles for bipedal gait and fine motility. Paget's disease: bones for bipedal gait and cranium. Understanding of the genetic mechanisms underlying the evolution of these recent human brain regions and paleoneurology my be the key to the focal, asymmetrical or systemic character of neurodegeneration, the pathologic heterogeneity/overlap of syndromic presentations associating gait, hand, language, cognition, mood and behaviour disorders.
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PMID:Paleoneurology: neurodegenerative diseases are age-related diseases of specific brain regions recently developed by Homo sapiens. 1870 90

This paper examines the issue of what the self is by reviewing neuropsychological research, which converges on the idea that the self may be more complex and differentiated than previous treatments of the topic have suggested. Although some aspects of self-knowledge such as episodic recollection may be compromised in individuals, other aspects-for instance, semantic trait summaries-appear largely intact. Taken together, these findings support the idea that the self is not a single, unified entity. Rather, it is a set of interrelated, functionally independent systems. Implications for understanding the self in various areas of psychological research-e.g., neuroimaging, autism, amnesia, Alzheimer's disease, and mirror self-recognition-are discussed in brief.
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PMID:The multiplicity of self: neuropsychological evidence and its implications for the self as a construct in psychological research. 2039 72

Samuel Beckett and Jorge Luis Borges have presented 20th century literature with a distinctive gallery of solitary figures who suffer from a series of physiological ailments: invalidism, decrepitude, infirmity and blindness, as well as neurological conditions such as amnesia and autism spectrum disorders. Beckett and Borges were concerned with the dynamics between illness and creativity, the literary representation of physical and mental disabilities, the processes of remembering and forgetting, and the inevitability of death. This article explores the depiction of physically and mentally disabled characters in Borges' Funes the Memorious (1942)--a story about an Uruguayan gaucho who has been left paralysed after a fall from a horse which simultaneously endowed him with an infallible memory and perception--and Beckett's Trilogy: Molloy (1951), Malone Dies (1951) and The Unnamable (1953). It examines the prodigious memory of Funes and the forgetful minds of Molloy and Malone with reference to influential neuropsychological studies such as Alexander Luria's twofold exploration of memory and forgetfulness in The Mind of a Mnemonist (1968) and The Man with a Shattered World (1972). The article demonstrates that in contrast to Beckett's amnesiacs and Luria's brain-damaged patient, who are able to transcend their circumstances through cathartic writing, Borges' and Luria's mnemonic prodigies fail to achieve anything significant with their unlimited memories and remain imprisoned within their cognitive disabilities. It reveals that medical discourses can provide invaluable insights and lead to a deeper understanding of the minds and bodily afflictions of literary characters.
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PMID:Literature and disability: the medical interface in Borges and Beckett. 2159 47

Visual object recognition is an essential accomplishment of advanced brains. Object recognition needs to be tolerant, or invariant, with respect to changes in object position, size, and view. In monkeys and humans, a key area for recognition is the anterior inferotemporal cortex (ITa). Recent neurophysiological data show that ITa cells with high object selectivity often have low position tolerance. We propose a neural model whose cells learn to simulate this tradeoff, as well as ITa responses to image morphs, while explaining how invariant recognition properties may arise in stages due to processes across multiple cortical areas. These processes include the cortical magnification factor, multiple receptive field sizes, and top-down attentive matching and learning properties that may be tuned by task requirements to attend to either concrete or abstract visual features with different levels of vigilance. The model predicts that data from the tradeoff and image morph tasks emerge from different levels of vigilance in the animals performing them. This result illustrates how different vigilance requirements of a task may change the course of category learning, notably the critical features that are attended and incorporated into learned category prototypes. The model outlines a path for developing an animal model of how defective vigilance control can lead to symptoms of various mental disorders, such as autism and amnesia.
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PMID:On the road to invariant recognition: explaining tradeoff and morph properties of cells in inferotemporal cortex using multiple-scale task-sensitive attentive learning. 2166 28

The olfactory mucosa, located in the nasal cavity, is in charge of detecting odours. It is also the only nervous tissue that is exposed to the external environment and easily accessible in every living individual. As a result, this tissue is unique for anyone aiming to identify molecular anomalies in the pathological brain or isolate adult stem cells for cell therapy. Molecular abnormalities in brain diseases are often studied using nervous tissue samples collected post-mortem. However, this material has numerous limitations. In contrast, the olfactory mucosa is readily accessible and can be biopsied safely without any loss of sense of smell(1). Accordingly, the olfactory mucosa provides an "open window" in the adult human through which one can study developmental (e.g. autism, schizophrenia)(2-4) or neurodegenerative (e.g. Parkinson, Alzheimer) diseases(4,5). Olfactory mucosa can be used for either comparative molecular studies(4,6) or in vitro experiments on neurogenesis(3,7). The olfactory epithelium is also a nervous tissue that produces new neurons every day to replace those that are damaged by pollution, bacterial of viral infections. This permanent neurogenesis is sustained by progenitors but also stem cells residing within both compartments of the mucosa, namely the neuroepithelium and the underlying lamina propria(8-10). We recently developed a method to purify the adult stem cells located in the lamina propria and, after having demonstrated that they are closely related to bone marrow mesenchymal stem cells (BM-MSC), we named them olfactory ecto-mesenchymal stem cells (OE-MSC)(11). Interestingly, when compared to BM-MSCs, OE-MSCs display a high proliferation rate, an elevated clonogenicity and an inclination to differentiate into neural cells. We took advantage of these characteristics to perform studies dedicated to unveil new candidate genes in schizophrenia and Parkinson's disease(4). We and others have also shown that OE-MSCs are promising candidates for cell therapy, after a spinal cord trauma(12,13), a cochlear damage(14) or in an animal models of Parkinson's disease(15) or amnesia(16). In this study, we present methods to biopsy olfactory mucosa in rats and humans. After collection, the lamina propria is enzymatically separated from the epithelium and stem cells are purified using an enzymatic or a non-enzymatic method. Purified olfactory stem cells can then be either grown in large numbers and banked in liquid nitrogen or induced to form spheres or differentiated into neural cells. These stem cells can also be used for comparative omics (genomic, transcriptomic, epigenomic, proteomic) studies.
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PMID:Isolating nasal olfactory stem cells from rodents or humans. 2187 29


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