Neuroscience letters
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Neuroscience letters · Jan 2019
Observational StudyDiagnostic value of NT-proCNP compared to NSE and S100B in cerebrospinal fluid and plasma of patients with sepsis-associated encephalopathy.
Sepsis-associated encephalopathy (SAE) has significant impact on the neurocognitive outcome of sepsis survivors. This study was conducted to analyze the amino-terminal propeptide of the C-type natriuretic peptide (NT-proCNP) as a biomarker for SAE in comparison to neuron-specific enolase (NSE) and S100B protein. Cerebrospinal fluid (CSF) and plasma samples from twelve septic patients with SAE and nine non-septic controls without encephalopathy were analyzed. ⋯ In the sepsis cohort CSF NT-proCNP levels correlated with CSF Interleukin-6 (IL-6) levels (r = 0.616, p < 0.05) and systemic inflammation represented by high plasma procalcitonin (PCT) levels at day 3 (r = 0.727, p < 0.05). The high peak concentration of plasma NT-proCNP in the early phase of sepsis might help to predict the emergence of SAE during the further course of disease. NT-proCNP in plasma might, in contrast to CSF, indicate neurological impairment in patients with SAE.
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Neuroscience letters · Jan 2019
Randomized Controlled TrialDistinct behavioral response of primary motor cortex stimulation in itch and pain after burn injury.
It is still unclear whether chronic neuropathic pain and itch share similar neural mechanisms. They are two of the most commonly reported challenges following a burn injury and can be some of the most difficult to treat. Transcranial direct current stimulation (tDCS) has previously been studied as a method to modulate pain related neural circuits. ⋯ We did not find any treatment effects during Phase II. Based on these findings, it seems that an important placebo effect occurred during sham tDCS for itch, while active M1 tDCS seems to disrupt sensory compensatory mechanisms. We hypothesize that pain and itch are complementary but distinct mechanisms of adaptation after peripheral sensory injury following a burn injury and need to be treated differently.
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Neuroscience letters · Jan 2019
Intrathecal administration of adrenomedullin induces mechanical allodynia and neurochemical changes in spinal cord and DRG.
This study investigated the effect of adrenomedullin (AM) on mechanical pain sensitivity and its possible mechanisms. Intrathecal injection of AM receptor agonist AM1-50 (20 μg) once per day briefly reduced mechanical pain threshold on days 1 and 2 but induced prolonged mechanical allodynia on day 3. However, AM1-50 did not change mechanical pain sensation when the AM receptor antagonist AM22-52 (20 μg) was intrathecally co-administered. ⋯ These results suggest that the increased AM bioactivity induced mechanical allodynia and may contribute to the mechanical pain hypersensitivity under pathological conditions. The mechanisms may involve the activation of ERK signaling pathway and spinal glia as well as the recruitment of nNOS and TRPV1 in the spinal dorsal horn or DRG. The present study indicates that inhibition of the activation AM receptor might provide a fruitful strategy to relieving chronic pain.
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Neuroscience letters · Jan 2019
ReviewWhy do so many genetic insults lead to Purkinje Cell degeneration and spinocerebellar ataxia?
The genetically heterozygous spinocerebellar ataxias are all characterized by cerebellar atrophy and pervasive Purkinje Cell degeneration. Up to date, more than 35 functionally diverse spinocerebellar ataxia genes have been identified. ⋯ In this review, we discuss the current consensus on shared mechanisms underlying the pervasive Purkinje Cell loss in spinocerebellar ataxia. Additionally, using recently published cell type specific expression data, we identified several Purkinje Cell-specific genes and discuss how the corresponding pathways might underlie the vulnerability of Purkinje Cells in response to the diverse genetic insults causing spinocerebellar ataxia.