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

T-type calcium channels are important modulators of both membrane potential and intracellular Ca(2+) concentration, allowing them to play key roles in such diverse processes as aldosterone production from adrenal glomerulosa cells to boosting pain signals in nociceptors. In both these examples, the Ca(v)3.2 isoform mediates Ca(2+) influx. This isoform is also of particular interest because mutations in its gene (CACNA1H) that enhance channel activity have been associated with idiopathic generalized epilepsies, whereas mutations that disrupt its activity have been associated with autism spectrum disorders. Block of T-channel activity has been proposed to contribute to the therapeutic usefulness of a wide variety of drugs, such as antihypertensives, antipsychotics, and antidepressants. Recent evidence strongly supports the hypothesis that block of Ca(v)3.2 channels might be useful in the treatment of neuropathic pain. Therefore, it is of particular interest that Ca(v)3.2 channels are exquisitely regulated by G protein-coupled receptors and various downstream effectors. This Perspective summarizes recent findings (p. 202) on this regulation and the novel pathways specifically activated by either neurokinin I, corticotropin-releasing factor receptor 1, or dopamine D(1) receptors.
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PMID:G protein-mediated inhibition of Cav3.2 T-type channels revisited. 1990 27

Schultz et al (2008) raised the question whether regression into autism is triggered, not by the measles-mumps-rubella (MMR) vaccine, but by acetaminophen (Tylenol) given for its fever and pain. Considerable evidence supports this contention, most notably the exponential rise in the incidence of autism since 1980, when acetaminophen began to replace aspirin for infants and young children. The impetus for this shift - a Centers for Disease Control and Prevention warning that aspirin was associated with Reye's syndrome - has since been compellingly debunked. If aspirin is not to be feared as a cause of Reyes syndrome, and acetaminophen is to be feared as a cause of autism, can the autism epidemic be reversed by replacing acetaminophen with aspirin or other remedies?
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PMID:Did acetaminophen provoke the autism epidemic? 2003 Apr 62

For many years the neuromodulator adenosine has been recognized as an endogenous anticonvulsant molecule and termed a "retaliatory metabolite." As the core molecule of ATP, adenosine forms a unique link between cell energy and neuronal excitability. In parallel, a ketogenic (high-fat, low-carbohydrate) diet is a metabolic therapy that influences neuronal activity significantly, and ketogenic diets have been used successfully to treat medically-refractory epilepsy, particularly in children, for decades. To date the key neural mechanisms underlying the success of dietary therapy are unclear, hindering development of analogous pharmacological solutions. Similarly, adenosine receptor-based therapies for epilepsy and myriad other disorders remain elusive. In this review we explore the physiological regulation of adenosine as an anticonvulsant strategy and suggest a critical role for adenosine in the success of ketogenic diet therapy for epilepsy. While the current focus is on the regulation of adenosine, ketogenic metabolism and epilepsy, the therapeutic implications extend to acute and chronic neurological disorders as diverse as brain injury, inflammatory and neuropathic pain, autism and hyperdopaminergic disorders. Emerging evidence for broad clinical relevance of the metabolic regulation of adenosine will be discussed.
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PMID:Adenosine, ketogenic diet and epilepsy: the emerging therapeutic relationship between metabolism and brain activity. 2019 Sep 67

Difficulties in social cognition are well recognized in individuals with autism spectrum conditions (henceforth 'autism'). Here we focus on one crucial aspect of social cognition: the ability to empathize with the feelings of another. In contrast to theory of mind, a capacity that has often been observed to be impaired in individuals with autism, much less is known about the capacity of individuals with autism for affect sharing. Based on previous data suggesting that empathy deficits in autism are a function of interoceptive deficits related to alexithymia, we aimed to investigate empathic brain responses in autistic and control participants with high and low degrees of alexithymia. Using functional magnetic resonance imaging, we measured empathic brain responses with an 'empathy for pain' paradigm assessing empathic brain responses in a real-life social setting that does not rely on attention to, or recognition of, facial affect cues. Confirming previous findings, empathic brain responses to the suffering of others were associated with increased activation in left anterior insula and the strength of this signal was predictive of the degree of alexithymia in both autistic and control groups but did not vary as a function of group. Importantly, there was no difference in the degree of empathy between autistic and control groups after accounting for alexithymia. These findings suggest that empathy deficits observed in autism may be due to the large comorbidity between alexithymic traits and autism, rather than representing a necessary feature of the social impairments in autism.
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PMID:Empathic brain responses in insula are modulated by levels of alexithymia but not autism. 2037 9

IgE-mediated allergic diseases (e.g., allergic rhinoconjunctivitis, atopic asthma and food allergy) are prevalent (up to 30%) in the general population and are increasing in developed countries. In infants and young children, non-IgE-mediated food allergy is also prevalent. In addition to easily recognized organ-specific symptoms, allergic diseases can cause neuropsychiatric symptoms, such as irritability and hyperactivity, in otherwise healthy individuals. This is also likely to occur in children with autism spectrum disorder (ASD). Moreover, the discomfort and pain associated with allergic diseases could aggravate behavioral symptoms in ASD children. Allergic conditions are easily treatable; however, ASD children may be underdiagnosed and/or undertreated for allergic and other common childhood diseases, in part due to their impaired communication skills. Practicing physicians should be aware of the potential impact of allergic diseases on behavioral symptoms and cognitive activity in ASD children. However, they also need to be aware that certain symptoms often attributed to 'allergy' by caregivers may not be immune mediated and should understand that behavioral symptoms can also be affected by many non-IgE-mediated causes.
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PMID:Autism spectrum disorders and allergy: observation from a pediatric allergy/immunology clinic. 2044 26

The study of the mechanism of acupuncture action was revolutionized by the use of functional magnetic resonance imaging (fMRI). Over the past decade, our fMRI studies of healthy subjects have contributed substantially to elucidating the central effect of acupuncture on the human brain. These studies have shown that acupuncture stimulation, when associated with sensations comprising deqi, evokes deactivation of a limbic-paralimbic-neocortical network, which encompasses the limbic system, as well as activation of somatosensory brain regions. These networks closely match the default mode network and the anti-correlated task-positive network described in the literature. We have also shown that the effect of acupuncture on the brain is integrated at multiple levels, down to the brainstem and cerebellum. Our studies support the hypothesis that the effect of acupuncture on the brain goes beyond the effect of attention on the default mode network or the somatosensory stimulation of acupuncture needling. The amygdala and hypothalamus, in particular, show decreased activation during acupuncture stimulation that is not commonly associated with default mode network activity. At the same time, our research shows that acupuncture stimulation needs to be done carefully, limiting stimulation when the resulting sensations are very strong or when sharp pain is elicited. When acupuncture induced sharp pain, our studies show that the deactivation was attenuated or reversed in direction. Our results suggest that acupuncture mobilizes the functionally anti-correlated networks of the brain to mediate its actions, and that the effect is dependent on the psychophysical response. In this work we also discuss multiple avenues of future research, including the role of neurotransmitters, the effect of different acupuncture techniques, and the potential clinical application of our research findings to disease states including chronic pain, major depression, schizophrenia, autism, and Alzheimer's disease.
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PMID:Acupuncture, the limbic system, and the anticorrelated networks of the brain. 2049 27

The purpose of the present article was to assess the available literature concerning pain and autism. First, authors summarized the published articles on pain reactivity in people with autism. Second, the hypotheses envisaged to explain the presence of expressive particularities in people with autism spectrum disorders were reviewed; these included endogenous opioid excess theory, sensorial abnormalities and sociocommunicative deficit. Finally, the present review dealt with the tools available to assess and manage pain in people with autism. In conclusion, the authors revealed the need for more research to obtain more consensual data and provided some recommendations in this domain that were under exploited by the scientific community. From a clinical point of view, more knowledge about pain in people with autism should enable the development of specific assessment tools and, consequently, better pain management in daily care.
Pain Res Manag
PMID:[Autism and pain - a literature review]. 2080 70

The cerebellum has long been considered quite separate from the neocortex, and accordingly the understanding of its role has been limited. Recent work has revealed that the cerebellum interacts regularly with the forebrain and it is involved in mood and cognition. In this article, the authors discuss an extensive system of neural circuits connecting the prefrontal, temporal, posterior parietal, and limbic cortices with the cerebellum. Language functions of the cerebellum are described, as well as cerebellar syndromes affecting cognition. The roles of the cerebellum in pain perception, attention deficit disorder, autism, dementia, and schizophrenia are discussed. Practical observations and tests to assess cerebellar function in the psychiatrist's office are described.
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PMID:Psychiatry, neurology, and the role of the cerebellum. 2094 51

We used National Fragile X Survey data in order to examine reported self-injurious behavior (SIB) to (a) generate lifetime and point prevalence estimates, (b) document detailed features of SIB (frequency, types, location, severity) in relation to gender, and (c) compare comorbid conditions between matched pairs (SIB vs. no SIB). Results indicate significant gender differences in frequency, topography, and location of SIB as well as sleep difficulties, comorbid conditions, pain sensitivity, and seizures. Matched pair comparisons (SIB vs. no SIB) revealed differences for males in sensory and attention problems, hyperactivity, aggression, autism, and anxiety and for females, in autism, attention, and anxiety. These results further clarify gender differences as well as comorbidity patterns between children with fragile X syndrome with and without SIB.
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PMID:Self-injurious behavior and fragile X syndrome: findings from the national fragile X survey. 2094

The Royal Society of Chemistry Biotechnology Group and Chemical Biology Interface Forum held a 1-day symposium, on April 19, 2010, on Chemical and Biological Therapeutic Approaches to Neurological Disorders, at the Royal Society of Chemistry, Burlington House, London. The purpose of the meeting, organized by Colin Bedford, Irene Francois and Klaus Rumpel, was to give an update of new developments regarding the genetics, biochemistry and pathophysiology of the major neurological disorders. These developments should facilitate the discovery of better clinical biomarkers and improved medicines for the diagnosis, monitoring and treatment of patients with neurological disease. The presentations and posters covered neurological disorders including Parkinson's disease, Alzheimer's disease, multiple sclerosis, schizophrenia, autism, epilepsy and pain. The majority of these psychiatric and neurological disorders cause long-term suffering and disability and thus create an important global public health problem. This was the central issue of a participative discussion that took place at the end of the meeting.
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PMID:Chemical & biological therapeutic approaches to neurological disorders. 2103 Nov 69


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