J Integr Neurosci
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The two most common surgical interventions for spontaneous intracerebral hemorrhage in the basal ganglia of patients more than 65 years old are either minimally invasive puncture and drainage or craniotomy. This study aimed to compare the curative effects of these two procedures in such patients. A retrospective study of patients older than years with spontaneous intracerebral hemorrhage was conducted between January 2012 and December 2015. ⋯ One year after surgery no statistically significant difference was observed between the two groups with respect to: evacuation rate of the hematoma five days after the operation, volume of residual hematoma, occurrence of rebleeding, development of infectious meningitis, length of hospitalization, fatality, or Glasgow Outcome Scale and Barthel Index scores. However, the amount of blood loss during the procedure (P < 0.001), total cost of hospitalization (P = 0.004), and incidence of epilepsy (P = 0.045) were significantly higher for the craniotomy group than the minimally invasive puncture and drainage group. It was found that, in patients older than 65 years with basal ganglia hemorrhage, minimally invasive puncture and drainage is less invasive, more cost efficient and induces less bleeding during surgery than craniotomy.
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Temporal lobe epilepsy is the most common form of epilepsy. However, for this type of condition, antiseizure medication is not effective for children. As miRNAs are involved in the development of temporal lobe epilepsy in children, they may provide potential therapeutic approaches for treatment. ⋯ Moreover, miR-135a-5p mediated the pro-apoptotic effect of temporal lobe epilepsy via repressing caspase activity and apoptosis inhibitor 1 expression. Additionally, miR-135a-5p reduced cell survival in the temporal lobe epilepsy condition. Overexpression of miR-135a-5p induced cell apoptosis through inhibition of caspase activity and apoptosis inhibitor 1 expression and suppressed cell survival in children with temporal lobe epilepsy.
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The advancement in medical research and intelligent modeling techniques has lead to the developments in anaesthesia management. The present study is targeted to estimate the depth of anaesthesia using cognitive signal processing and intelligent modeling techniques. The neurophysiological signal that reflects cognitive state of anaesthetic drugs is the electroencephalogram signal. ⋯ The Kruskal-Wallis statistical test is applied on the relative wave energy features to check the discriminating capability of relative wave energy features as awake, light anaesthesia, moderate anaesthesia and deep anaesthesia. A novel depth of anaesthesia index is generated by implementing a Adaptive neuro-fuzzy inference system based fuzzy c-means clustering algorithm which uses relative wave energy features as inputs. Finally, the generated depth of anaesthesia index is compared with a commercially available depth of anaesthesia monitor Bispectral index.
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The present review attempts to put together the available evidence and potential research paradigms at the interface of obstructive sleep apnea syndrome (OSAS), sleep micro- and macrostructure, cerebral vasoreactivity and cognitive neuroscience. Besides the significant health-related consequences of OSAS including hypertension, increased risk of cardio- and cerebrovascular events, notable neurocognitive lapses and excessive daytime somnolence are considered as potential burdens. The intermittent nocturnal hypoxia and hypercapnia which occur in OSAS are known to affect cerebral circulation and result in brain hypoperfusion. ⋯ This is proposed to be related to an upregulated proinflammatory state which may potentially result in apoptotic cell loss in the brain. On this basis, a pragmatic framework of the possible neural mechanisms which underpin obstructive sleep apnea-related neurocognitive decline has been discussed in this review. In addition, the impact of OSAS on cerebral autoregulation and sleep microstructure has been articulated.
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Chronic morphine exposure leads to tolerance, which limits the clinical use of this potent analgesic in the treatment of severe and chronic pain. Compelling evidence suggest that neuro-immune activation (pro-inflammatory cytokines including IL-1β, IL-6 and TNF) as well as neuro-inflammation have been shown to mediate the development of morphine analgesic tolerance. Toll-like receptors (TLRs), especially TLR-4, have also been reported to contribute to the development of morphine analgesic tolerance. ⋯ Hence, we hypothesis the possible involvement of myeloid differentiation primary response protein 88 (MyD88), a key adaptor protein for the TLR and IL-1R families, in the development of tolerance to morphine-induced analgesia. Our study demonstrated that chronic intrathecal morphine injection led to a robust increase of MyD88 expression in rat spinal cord. Sustained elevation of MyD88 may play a role in modulating the development of morphine antinociceptive tolerance.