7 research outputs found
Multi-modal magnetic resonance imaging in the acute and sub-acute phase of mild traumatic brain injury: can we see the difference?
Advanced magnetic resonance imaging (MRI) methods were shown to be able to detect the subtle structural consequences of mild traumatic brain injury (mTBI). The objective of this study was to investigate the acute structural alterations and recovery after mTBI, using diffusion tensor imaging (DTI) to reveal axonal pathology, volumetric analysis, and susceptibility weighted imaging (SWI) to detect microhemorrhage. Fourteen patients with mTBI who had computed tomography with negative results underwent MRI within 3 days and 1 month after injury. High resolution T1-weighted imaging, DTI, and SWI, were performed at both time points. A control group of 14 matched volunteers were also examined following the same imaging protocol and time interval. Tract-Based Spatial Statistics (TBSS) were performed on DTI data to reveal group differences. T1-weighted images were fed into Freesurfer volumetric analysis. TBSS showed fractional anisotropy (FA) to be significantly (corrected p<0.05) lower, and mean diffusivity (MD) to be higher in the mTBI group in several white matter tracts (FA=40,737; MD=39,078 voxels) compared with controls at 72 hours after injury and still 1month later for FA. Longitudinal analysis revealed significant change (i.e., normalization) of FA and MD over 1 month dominantly in the left hemisphere (FA=3408; MD=7450 voxels). A significant (p<0.05) decrease in cortical volumes (mean 1%) and increase in ventricular volumes (mean 3.4%) appeared at 1 month after injury in the mTBI group. SWI did not reveal microhemorrhage in our patients. Our findings present dynamic micro- and macrostructural changes occurring in the acute to sub-acute phase in mTBI, in very mildly injured patients lacking microhemorrhage detectable by SWI. These results underscore the importance of strictly defined image acquisition time points when performing MRI studies on patients with mTBI
Serum L-arginine and Dimethylarginine Levels in Migraine Patients with Brain White Matter Lesions
Background/Aim Migraine is a risk factor for the formation of silent brain white matter lesions (WMLs) that are possibly ischemic in nature. Although dysfunction of the L-arginine/nitric oxide (NO) pathway has been associated with oxidative stress and endothelial dysfunction in migraine, its role in WML development has not been specifically investigated. Thus, this prospective study aimed to measure the serum concentrations of the NO substrate L-arginine, the NO synthase inhibitor asymmetric dimethylarginine (ADMA), and the L-arginine transport regulator symmetric dimethylarginine (SDMA) in migraine patients in a headache-free period. Methods All participants underwent MR imaging to assess for the presence of WMLs on fluid-attenuated inversion recovery imaging. Altogether 109 migraine patients (43 with lesions, 66 without lesions) and 46 control individuals were studied. High-performance liquid chromatography was used to quantify L-arginine, ADMA and SDMA serum concentrations. Migraine characteristics were investigated, and participants were screened for risk factors that can lead to elevated serum ADMA levels independent of migraine. Results Migraine patients and controls did not differ in regard to vascular risk factors. Migraineurs with WMLs had a longer disease duration ( p < 0.001) and a higher number of lifetime headache attacks ( p = 0.005) than lesion-free patients. Higher L-arginine serum levels were found in both migraine subgroups compared to controls ( p < 0.001). Migraine patients with WMLs showed higher ADMA concentrations than lesion-free patients and controls ( p < 0.001, for both). In migraineurs, the presence of WMLs, aura and increasing age proved to be significant predictors of increased ADMA levels ( p = 0.008, 0.047 and 0.012, respectively). SDMA serum levels of lesional migraineurs were higher than in nonlesional patients ( p < 0.001). The presence of lesions and increasing age indicated an increased SDMA level ( p = 0.017 and 0.001, respectively). Binary logistic regression analysis showed that ADMA level ( p = 0.006), increasing age ( p = 0.017) and the total number of lifetime migraine attacks ( p = 0.026) were associated with an increased likelihood of exhibiting WMLs. There was no significant effect of age on ADMA and SDMA concentrations in controls. Conclusions Elevated ADMA levels may impact the pathogenesis of migraine-related WMLs by influencing cerebrovascular autoregulation and vasomotor reactivity. Higher SDMA concentrations may indirectly influence NO synthesis by reducing substrate availability. Elevated L-arginine serum levels might reflect an increased demand for NO synthesis. </jats:sec
Az acetilszalicilsav-rezisztencia klinikai jelentősége cerebrovascularis betegek esetében
Az elmĂşlt Ă©vekben egyre több tanulmány foglalkozott az acetilszalicilsav- rezisztencia fogalmával Ă©s lehetsĂ©ges klinikai következmĂ©nyeivel. BETEGEK ÉS MĂ“DSZEREK - 281, krĂłnikus cerebrovascularis beteg vett rĂ©szt a tanulmányunkban. A betegeket kĂ©t csoportra osztottuk optikai aggregometriás leletĂĽk alapján (acetilszalicilsav-reszponder vs. -rezisztens). Ă–sszehasonlĂtottuk a kĂ©t csoport rizikĂłprofilját, szedett gyĂłgyszereit, laboratĂłriumi paramĂ©tereit Ă©s klinikai kimenetelĂ©t. EREDMÉNYEK - Az acetilszalicilsav-rezisztens betegek között magasabb volt a nĹ‘k aránya [(23 (45,1%) vs. 92 (40%) (p<0,05)], továbbá gyakoribb volt a dohányzás (38% vs. 25%), hypertonia (92 vs. 78%), hypercholesterinaemia (5,69 vs. 4,85 mmol/l), magasabb LDL- (3,71 vs. 2,85 mmol/l) Ă©s trigliceridĂ©rtĂ©kek (2,78 vs. 1,97 mmol/l), továbbá magasabb hsCRPszint (17,89 vs. 7,09 mmol/l) (p<0,01). A statinok használata (56% vs. 36%) gyakoribb volt a reszpondercsoportban (p<0,01). Az agonisták által kiváltott thrombocytaaggregáciĂłs Ă©rtĂ©kek szoros összefĂĽggĂ©st mutattak a koleszterin-, LDL-, triglicerid- Ă©s hsCRP-Ă©rtĂ©kekkel (p<0,05). KedvezĹ‘tlen kimenetel 13 (25,5%) acetilszalicilsav-nonreszponder Ă©s 32 (13,9%) acetilszalicilsavreszponder beteg esetĂ©ben lĂ©pett fel (p<0,01). MultivariáciĂłs analĂzis során azonban a dohányzás (OR: 2,38, CI: 1,77- 5,44), az emelkedett LDL- (OR: 3,01, CI: 2,34-5,67) Ă©s emelkedett hsCRP-Ă©rtĂ©kek (OR: 2,44, CI: 1,55-7,02) (p<0,05) voltak a kedvezĹ‘tlen vascularis kimenetel fĂĽggetlen rizikĂłfaktorai. KĂ–VETKEZTETÉS - Tanulmányunk eredmĂ©nyei alapján az acetilszalicilsav-rezisztencia kedvezĹ‘tlenebb klinikai kimenetellel járt egyĂĽtt, de nem volt a jövĹ‘beli vascularis esemĂ©nyek fĂĽggetlen rizikĂłfaktora. EredmĂ©nyeink felvetik a nem megfelelĹ‘ prevenciĂłs kezelĂ©s szerepĂ©t a jelensĂ©g hátterĂ©ben
Bi-exponential diffusion signal decay in normal appearing white matter of multiple sclerosis.
PURPOSE
Our aim was to characterize bi-exponential diffusion signal changes in normal appearing white matter of multiple sclerosis (MS) patients.
METHODS
Diffusion parameters were measured using mono-exponential (0-1000 s/mm(2)) and bi-exponential (0-5000 s/mm(2)) approaches from 14 relapsing-remitting subtype of MS patients and 14 age- and sex-matched controls after acquiring diffusion-weighted images on a 3T MRI system. The results were analyzed using parametric or nonparametric tests and multiple linear regression models.
RESULTS
Mono-exponential apparent diffusion coefficient (ADC) slightly increased in controls (P=.09), but decreased significantly in MS as a function of age, nonetheless an elevated ADC was observed with increasing lesion number in patients. Bi-exponential analyses showed that the increased ADC is the result of decreased relative volume fraction of slow diffusing component (f(s)). However, the fast and slow diffusion components (ADC(f), ADC(s)) did not change as a function of either age in controls or lesion number and age in MS patients.
CONCLUSIONS
These data demonstrated that the myelin content of the white matter affects diffusion in relapsing-remitting subtype of multiple sclerosis that is possibly a consequence of the shift between different water fractions