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BACKGROUND: The neurological effect of viral respiratory infections has been acknowledged in many studies. However, patients who recovered from this infection show neurological manifestations and are not being routinely transferred for electrodiagnostic evaluation. AIM: This study aimed to examine the neurological effect of viral respiratory infections on the nerve function using electrophysiology in patients fully recovered from viral respiratory infections. METHODS: To limit bias in the results, the authors decided to choose patients who recovered from one virus in all participants (coronavirus). Medical records were screened for patients who performed nerve conduction studies (NCSs) before the coronavirus pandemic. Thirty patients met our inclusion criteria, and only 10 showed up to perform NCS. Data of the NCS was compared before and after the coronavirus infection for motor and sensory NCS parameters. RESULTS: An increase in both the median and ulnar sensory nerve latencies and a decrease in the sensory nerve amplitude was observed. Also, there was a decrease in the motor conduction velocity (MCV) of the ulnar nerves and motor amplitude in the median nerve. In the lower limbs, there was a decrease in the sural nerve latency, increased MCV in the tibial nerves, and decreased MCV in the peroneal nerves. The proximal amplitudes of the tibial and peroneal nerves were increased, but the distal amplitude was increased only in the peroneal nerves and decreased in the tibial nerves. CONCLUSION: There is a significant impact of viral infections on the peripheral nerves. Large-scale prospective studies are required to investigate the pathogenesis of the neuropathy and myopathy after viral infections.
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Cognitive impairment is among the most challenging characteristics of autism spectrum disorder (ASD). Although ASD is one of the common neurodevelopmental disorders, we are still behind in diagnosing and treating cognitive impairment in ASD. Cognitive impairment in ASD varies, meaning it could be at the sensory perception level to cognitive processing, learning, and memory. There are no diagnostic criteria for cognitive impairment that are specific to ASD. The leading causes of cognitive impairment in ASD could be neurological, immune, and gastrointestinal dysfunction. Immune dysfunction might lead to neuroinflammation, affecting neural connectivity, glutamate/gamma-aminobutyric acid (GABA) balance, and plasticity. The gut-brain axes are essential in the developing brain. Special retinal changes have recently been detected in ASD, which need clinical investigation to find their possible role in early diagnosis. Early intervention is crucial for ASD cognitive dysfunction. Due to the heterogeneity of the disease, the clinical manifestation of ASD makes it difficult for clinicians to develop gold-standard diagnostic and therapeutic criteria. We suggest a triad for diagnosis, which includes clinical tests for immune and gastrointestinal dysfunction biomarkers, clinical examination for the retina, and an objective neurocognitive evaluation for ASD, and to develop a treatment strategy involving these three aspects. Developing clear treatment criteria for cognitive impairment for ASD would improve the quality of life of ASD people and their caregivers and would delay or prevent dementia-related disorders in ASD people.
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BACKGROUND: Autism spectrum disorder (ASD) encompasses a group of disorders characterized by difficulties with social interaction and repetitive behavior. The condition is supposed to originate from early shifts in brain development, while the underlying processes are unknown. Moreover, a considerable number of patients with ASD experience digestive difficulties. Metalloproteases (ADAMs) are a class of enzymes capable of cleaving membrane-bound proteins. Members of this family, ADAM17 and ADAM22, have the ability to cleave proteins like the pro-inflammatory cytokine TNF-ά and glutamate synaptic molecules, which are both engaged in neuro-inflammation and glutamate excitotoxicity as crucial etiological mechanisms in ASD. ADAM17 and ADAM22 may also have a role in ASD microbiota-gut-brain axis connections by regulating immunological and inflammatory responses in the intestinal tract. SUBJECTS AND METHODS: Using ELISA kits, the plasma levels of ADAM17 and ADAM22 were compared in 40 children with ASD and 40 typically developing children. All of the autistic participants' childhood autism rating scores (CARS), social responsiveness scales (SRS), and short sensory profiles (SSP) were evaluated as indicators of ASD severity. RESULTS: Our results showed that plasma levels of ADAM17 were significantly lower in ASD children than in control children, while ADAM22 demonstrated non-significantly lower levels. Our data also indicate that while ADAM17 correlates significantly with age, ADAM22 correlates significantly with CARS as a marker of ASD severity. CONCLUSIONS: Our interpreted data showed that alteration in ADAM17 and ADAM22 might be associated with glutamate excitotoxicity, neuroinflammation, and altered gut microbiota as etiological mechanisms of ASD and could be an indicator of the severity of the disorder.
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Although autism spectrum disorder (ASD) is a common developmental disorder, primary healthcare providers show a deficit in providing early diagnosis. To understand parents' experience and perspective in the diagnosis and intervention process of their children, a survey was deployed through social media to parents' with at least one child diagnosed with ASD. The survey included parents experience, satisfaction and perception in the diagnosis process and services provided for their children, stigma and type of support received. A total of 223 participants were enrolled. Although 62% of ASD patients were diagnosed by three years old, most diagnoses (66%) were non-physician initiated. Additionally, 40.8% of the parents reported that the services required for their child are available in their area of residence, but only 7.9% were satisfied with these services. Parents who received psychological support (9.9%) started early intervention, and their children have a better prognosis (p ≤ 0.005). Stigmatized parents were more likely to delay intervention (p ≤ 0.005). Parents' perception is to have qualified healthcare and educational professionals experienced in ASD. Our findings suggest that a specialized family-centred medical home for ASD patients would significantly benefit ASD patients, increase parents' satisfaction, reduce parents' stress, and ease their children's transition to adolescents.
