Journal of the neurological sciences
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A modified Marmarou impact acceleration model was used to help screen biomarkers to assess brain injury severity. Anesthetized male Sprague-Dawley rats were subjected to a closed head injury from 1.25, 1.75 and 2.25 m drop heights. Linear and angular responses of the head were measured in vivo. 24h after impact, cerebrospinal fluid (CSF) and serum were collected. ⋯ Levels of Aβ were not significantly different between groups. Pearson's correlation analysis showed pNF-H and GFAP levels in CSF and serum had positive correlation with power (rate of impact energy), followed by average linear acceleration and surface righting (p<0.01), which were good predictors for traumatic axonal injury according to histologic assessment in our previous study, suggesting that they are directly related to the injury mechanism. The model used in this study showed a unique ability in elucidating the relationship between biomarker levels and severity of the mechanical trauma to the brain.
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Hypomimia which refers to a reduced degree in facial expressiveness is a common sign in Parkinson's disease (PD). The objective of our study was to investigate how hypomimia affects PD patients' facial expression of pain. The facial expressions of 23 idiopathic PD patients in the Off-phase (without dopaminergic medication) and On-phase (after dopaminergic medication intake) and 23 matched controls in response to phasic heat-pain and a temporal summation procedure were recorded and analyzed for overall and specific alterations using the Facial Action Coding System (FACS). ⋯ Not only overall quantitative changes in the degree of facial pain expressiveness occurred in PD patients but also qualitative changes were found. The latter refer to a strongly affected encoding of the sensory dimension of pain (eye-narrowing) while the encoding of the affective dimension of pain (contradiction of the eyebrows) was preserved. This imbalanced pain signal might affect pain communication and pain assessment.
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Cell apoptosis is involved in acute brain injury after aneurysmal subarachnoid hemorrhage (aSAH). The protein cytokeratin-18 (CK-18) is cleaved by the action of caspases during apoptosis, and the resulting fragments are released into the blood as caspase-cleaved CK (CCCK)-18. Our study examined the relationship between circulating CCCK-18 levels and long-term clinical outcomes among aSAH patients. ⋯ High circulating CCCK-18 levels were associated with injury severity and a poor clinical outcome after aSAH and CCCK-18 had the potential to be a good prognostic biomarker for aSAH.
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Restless legs syndrome (RLS) is a common sleep disorder in which patients feel unpleasant leg sensations and the urge to move their legs during rest, particularly at night. Leg movement improves these symptoms. Although several studies have demonstrated an association between cardiovascular disease and RLS, the mechanisms underlying this relationship remain unclear. Recent studies have shown changes in the peripheral microvasculature, including altered blood flow and capillary tortuosity, and peripheral hypoxia. Vascular endothelial dysfunction can be assessed noninvasively with ultrasound measurements of brachial artery flow-mediated dilatation (FMD). Therefore, this study investigated FMD in RLS patients to determine the involvement of microvascular alterations in this disorder. ⋯ This study demonstrated that RLS patients have poorer vascular endothelial function than normal healthy subjects and provides further evidence supporting the involvement of peripheral systems in the generation of RLS.
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We have experimentally demonstrated that cobalamin (Cbl) deficiency increases normal cellular prion (PrP(C)) levels in rat spinal cord (SC) and cerebrospinal fluid (CSF), and decreases PrP(C)-mRNA levels in rat SC. Repeated intracerebroventricular administrations of anti-octapeptide repeat-PrP(C)-region antibodies to Cbl-deficient (Cbl-D) rats prevent SC myelin lesions, and the administrations of PrP(C)s to otherwise normal rats cause SC white matter lesions similar to those induced by Cbl deficiency. ⋯ We have clinically demonstrated that PrP(C) levels are increased in the CSF of patients with subacute combined degeneration (SCD), unchanged in the CSF of patients with Alzheimer's disease and amyotrophic lateral sclerosis, and decreased in the CSF and SC of patients with multiple sclerosis (MS), regardless of its clinical course. We conclude that SCD (human and experimental) is a neurological disease due to excess PrP(C) without conformational change and aggregation, that the increase in PrP(C) levels in SCD and Cbl-D polyneuropathy and their decrease in MS CNS make them antipodian myelin diseases in terms of quantitative PrP(C) abnormalities, and that these abnormalities are related to myelin damage in the former, and impede myelin repair in the latter.