Journal of the neurological sciences
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Olfactory dysfunction and REM sleep behavior disorder (RBD) are recognized as pre-motor symptoms of Parkinson's disease (PD). Cognitive dysfunction is observed at a high rate even in the early stages of PD as an important non-motor symptom. PD has been classified in different subtypes and it is unknown if olfactory dysfunction and RBD occur more often in one particular subtype. We investigated the relationship between olfactory impairment, RBD, initial cognitive performance and motor phenotype in PD. ⋯ Olfactory dysfunction and RBD differed according to the motor phenotypes of PD. This suggests that olfactory dysfunction and RBD might relate to prognosis in patients with PD. Patients who have both hyposmia and RBD were more likely to exhibit cognitive dysfunction.
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Our objective was to apply the technique of measuring diameters of optic nerve sheath (ONSD) for the intracranial pressure assessment for the cases with traumatic head injury without hemorrhage. In a retrospective study, CT data of 720 adult patients were collected and analyzed. ONSDs were measured at the point where the ophthalmic artery crosses the optic nerve (anatomical landmark) together with the eyeball transverse diameter (ETD). ⋯ ONSD/ETD ratio was 0.28±0.05 against 0.19±0.02 in healthy adults (p=0.02). We did not find correlation between ONSD/ETD ratio with initial Glasgow Coma Scale score but there was an inverse correlation between ONSD/ETD ratio and the Glasgow Outcome Score (r=-0.64). We conclude that in majority of cases with traumatic head injury without hemorrhage the ONSD is significantly enlarged indicating elevated intracranial pressure even if CT scans are negative.
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Previous studies have shown that xenon-delayed postconditioning for up to 2h after reperfusion provides protection against spinal cord ischemia/reperfusion (I/R) injury in rats. This study was designed to determine the roles of phosphatidylinositol 3-kinase (PI3K)-Akt and extracellular signal-regulated kinase (ERK) in this neuroprotection. The rats were randomly assigned to the following nine groups (n=16∗9): 1) I/R+N2 group, 2) I/R+Xe group, 3) I/R+PD98059+N2 group (ERK blocking agent), 4) I/R+wortmannin+N2 group (PI3K-Akt blocking agent), 5) I/R+PD98059+Xe group, 6) I/R+wortmannin+Xe group, 7) I/R+DMSO+Xe group (dimethyl sulfoxide, vehicle control), 8) I/R+DMSO+N2 group, and 9) sham group (no spinal cord ischemia and no xenon). ⋯ Compared with the I/R group, rats in the I/R+Xe group had higher neurological scores, more normal motor neurons, fewer apoptotic neurons and significantly higher levels of p-Akt and p-ERK at each time point (P<0.05). Compared with the I/R+Xe group, the I/R+PD98059+Xe and I/R+wortmannin+Xe groups showed worse neurological outcomes and less p-Akt and p-ERK at each time point (P<0.05). These results suggest that xenon-delayed postconditioning improves neurological outcomes to spinal cord I/R injury in rats through the activation of the AKT and ERK signaling pathways.
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Nociceptive abnormalities indicating increased pain sensitivity have been reported in patients with Parkinson's disease (PD). The disturbances are mostly responsive to dopaminergic (DA) treatment; yet, there are conflicting results. The objective of the present study was to investigate pain processing and nociception in PD patients in a more comprehensive manner than previous studies. For this purpose, a multi-methods approach was used in order to monitor different levels of the central nervous system (spinal, subcortical-vegetative, cortical). ⋯ Increased pain sensitivity (heat-pain threshold) in the Off which normalizes in the On argues for DA induced dysfunctions of the nigrostriatal pain loops with the basal ganglia as main circuit in our PD sample. Dysfunctions of the subcortical-vegetative parameters despite of inconspicuous cortical nociception suggest disturbances of the central or peripheral innervation of sympathetic branches with coincidently intact ascending pathways in the PD group.
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Intracranial bleeding and inflammatory reactions are common consequences of traumatic brain injury (TBI). Neutrophil gelatinase-associated lipocalin (NGAL), an iron-handling and acute phase protein, may participate in the pathogenesis of TBI. Therefore, we hypothesize that NGAL may be of high diagnostic and therapeutic relevance in the prognosis of TBI. ⋯ NGAL may be a novel biomarker reflecting TBI severity, which increased obviously and negatively correlated with GCS, TS, and RTS scores; additionally, this characteristic of NGAL may be helpful in guiding clinical TBI therapeutic strategies.