The effect of magnetic resonance imaging on mercury release from dental amalgam at 3T and 7T

Objectives To measure mercury release from standardised hydroxyapatite/amalgam constructs during MRI scanning and investigate the impact of static field strength and radiofrequency (RF) power on mercury release. Methods Amalgam was placed into 140 hydroxyapatite disks and matured for 14-days in artificial saliva. The solution was replaced, and samples split into five groups of 28 immediately prior to MRI. One group had no exposure, and the remainder were exposed to either a 3T or 7T MRI scanner, each at high and low RF power. Mercury concentration was measured by inductively coupled plasma mass spectrometry. Groups were compared using one-way ANOVA, and two-way ANOVA for main effects/ interaction of field strength/ RF power. Results Mercury concentration was increased in the 7T groups (high/ low: 15.43/ 11.33 ng mL−1) and 3T high group (3.59) compared to control (2.44). MRI field strength significantly increased mercury release (p < .001) as did RF power (p = .030). At 3T, mercury release was 20.3 times lower than during maturation of dental amalgam, and for the average person an estimated 1.50 ng kg−1 of mercury might be released during one 3T investigation; this is substantially lower than the tolerable weekly intake of 4,000 ng kg−1. Conclusion Mercury release from amalgam shows a measurable increase following MRI, and the magnitude changes with magnetic field strength and RF power. The amount of mercury released is small compared to release during amalgam maturation. Amalgam mercury release during MRI is unlikely to be clinically meaningful and highly likely to remain below safe levels

Hippocampal position and orientation as prognostic biomarkers for posttraumatic epileptogenesis: an experimental study in a rat lateral fluid percussion model

Objective This study was undertaken to identify prognostic biomarkers for posttraumatic epileptogenesis derived from parameters related to the hippocampal position and orientation. Methods Data were derived from two preclinical magnetic resonance imaging (MRI) follow-up studies: EPITARGET (156 rats) and Epilepsy Bioinformatics Study for Antiepileptogenic Therapy (EpiBioS4Rx; University of Eastern Finland cohort, 43 rats). Epileptogenesis was induced with lateral fluid percussion-induced traumatic brain injury (TBI) in adult male Sprague Dawley rats. In the EPITARGET cohort, T2*-weighted MRI was performed at 2, 7, and 21 days and in the EpiBioS4Rx cohort at 2, 9, and 30 days and 5 months post-TBI. Both hippocampi were segmented using convolutional neural networks. The extracted segmentation mask was used for a geometric construction, extracting 39 parameters that described the position and orientation of the left and right hippocampus. In each cohort, we assessed the parameters as prognostic biomarkers for posttraumatic epilepsy (PTE) both individually, using repeated measures analysis of variance, and in combination, using random forest classifiers. Results The extracted parameters were highly effective in discriminating between sham-operated and TBI rats in both the EPITARGET and EpiBioS4Rx cohorts at all timepoints (t; balanced accuracy &gt; .9). The most discriminating parameter was the inclination of the hippocampus ipsilateral to the lesion at t = 2 days and the volumes at t &gt;= 7 days after TBI. Furthermore, in the EpiBioS4Rx cohort, we could effectively discriminate epileptogenic from nonepileptogenic animals with a longer MRI follow-up, at t = 150 days (area under the curve = .78, balanced accuracy = .80, p = .0050), based on the orientation of both hippocampi. We found that the ipsilateral hippocampus rotated outward on the horizontal plane, whereas the contralateral hippocampus rotated away from the vertical direction. Significance We demonstrate that assessment of TBI-induced hippocampal deformation by clinically translatable MRI methodologies detects subjects with prior TBI as well as those at high risk of PTE, paving the way toward subject stratification for antiepileptogenesis studies

Comparison of Intravenous Esmolol and Oral Clonidine for Attenuation of Stress Response to Laryngoscopy and Intubation in Patients Undergoing Surgery under General Anesthesia: A Randomized Clinical Study

Introduction: Direct laryngoscopy and endotracheal intubation are the most noxious stimuli during induction of anaesthesia. Airway instrumentation frequently induces a cardiovascular stress response characterized by hypertension and tachycardia due to reflex sympathoadrenal discharge caused by epipharyngeal and parapharyngeal stimulation. Various pharmacological approaches have been used to attenuate the pressure responses to laryngoscopy and tracheal intubation e.g. volatile inhalational agents, lignocaine, opioids, sodium nitroprusside, nitroglycerine, calcium channel blockers, and adrenergic blockers (alpha -2 agonists and beta blockers).Objectives: The purpose of this study is to compare the efficacy and safety of i.v esmolol and oral clonidine in attenuating the changes of blood pressure and heart rate by tracheal intubation.Materials and Methods: 40 patients posted for various surgeries under general anesthesia were randomly divided into two groups. Group C subjects received Clonidine 150 mcg PO, 90 minutes prior to induction of anaesthesia where as Group E subjects received I.V Esmolol 0.5mg/kg 90 seconds prior to intubation. To maintain blinding, Group C patients received I.V 0.9% Normal saline 90 seconds prior to intubation where as Group E patients received placebo tablet containing multi vitamins 90 minutes prior to induction .HR, systolic blood pressure (SBP), diastolic blood pressure (DBP), Mean arterial pressure (MAP) , rate pressure product (RPP), Spo2, ECG will be recorded prior to induction (Base line), at the time of intubation and 1, 3, 5, and 10 min after intubation . Type of study: A randomized clinical study.Results: Pulse rate, SBP, DBP, MAP and RPP were comparable at baseline, at time of induction, during laryngoscopy and intubation and throughout whole study period it was not statistically significant in both groups (p&gt;0.05). However in Intergroup comparison, SBP was comparable at base line and after 5 min of laryngoscopy and intubation in both groups, but SBP was significantly higher after 1 and 3 min of laryngoscopy and intubation in Group E than Group C. Also, there was statistically significant increase in MAP following laryngoscopy and intubation at one min in Group E than Group C (P&lt;0.05). RPP was significantly higher after 1 and 3 min of laryngoscopy and intubation in Group E than Group C. Postoperative complications like dryness of mouth, excessive sedation, PONV, hypotension, Bradycardia, bronchospasm were not observed in any case in both groups. Conclusion: This study concluded that clonidine and esmolol provide hemodynamic stability but clonidine provides more stability with postoperative sedation

Diffusion MRI approaches for investigating microstructural complexity in a rat model of traumatic brain injury.

Our study explores the potential of conventional and advanced diffusion MRI techniques including diffusion tensor imaging (DTI), and single-shell 3-tissue constrained spherical deconvolution (SS3T-CSD) to investigate complex microstructural changes following severe traumatic brain injury in rats at a chronic phase. Rat brains after sham-operation or lateral fluid percussion (LFP) injury were scanned ex vivo in a 9.4 T scanner. Our region-of-interest-based approach of tensor-, and SS3T-CSD derived fixel-, 3-tissue signal fraction maps were sensitive to changes in both white matter (WM) and grey matter (GM) areas. Tensor-based measures, such as fractional anisotropy (FA) and radial diffusivity (RD), detected more changes in WM and GM areas as compared to fixel-based measures including apparent fiber density (AFD), peak FOD amplitude and primary fiber bundle density, while 3-tissue signal fraction maps revealed distinct changes in WM, GM, and phosphate-buffered saline (PBS) fractions highlighting the complex tissue microstructural alterations post-trauma. Track-weighted imaging demonstrated changes in track morphology including reduced curvature and average pathlength distal from the primary lesion in severe TBI rats. In histological analysis, changes in the diffusion MRI measures could be associated to decreased myelin density, loss of myelinated axons, and increased cellularity, revealing progressive microstructural alterations in these brain areas five months after injury. Overall, this study highlights the use of combined conventional and advanced diffusion MRI measures to obtain more precise insights into the complex tissue microstructural alterations in chronic phase of severe brain injury

Nonconvulsive status epilepticus in rats leads to brain pathology

Objective: Status epilepticus (SE) is an abnormally prolonged epileptic seizure that if associated with convulsive motor symptoms is potentially life threatening for a patient. However, 20%-40% of patients with SE lack convulsive events and instead present with more subtle semiology such as altered consciousness and less motor activity. Today, there is no general consensus regarding to what extent nonconvulsive SE (NCSE) is harmful to the brain, which adds uncertainty to stringent treatment regimes. Methods: Here, we evaluated brain pathology in an experimental rat and mouse model of complex partial NCSE originating in the temporal lobes with Western blot analysis, immunohistochemistry, and ex vivo diffusion tensor imaging (DTI). The NCSE was induced by electrical stimulation with intrahippocampal electrodes and terminated with pentobarbital anesthesia. Video-electroencephalographic recordings were performed throughout the experiment. Results: DTI of mice 7 weeks post-NCSE showed no robust long-lasting changes in fractional anisotropy within the hippocampal epileptic focus. Instead, we found pathophysiological changes developing over time when measuring protein levels and cell counts in extracted brain tissue. At 6 and 24 hours post-NCSE in rats, few changes were observed within the hippocampus and cortical or subcortical structures in Western blot analyses of key components of the cellular immune response and synaptic protein expression, while neurodegeneration had started. However, 1 week post-NCSE, both excitatory and inhibitory synaptic protein levels were decreased in hippocampus, concomitant with an excessive microglial and astrocytic activation. At 4 weeks, a continuous immune response in the hippocampus was accompanied with neuronal loss. Levels of the excitatory synaptic adhesion molecule N-cadherin were decreased specifically in rats that developed unprovoked spontaneous seizures (epileptogenesis) within 1 month following NCSE, compared to rats only exhibiting acute symptomatic seizures within 1 week post-NCSE. Significance: These findings provide evidence for a significant brain pathology following NCSE in an experimental rodent model

Acute Hippocampal Damage as a Prognostic Biomarker for Cognitive Decline but Not for Epileptogenesis after Experimental Traumatic Brain Injury

It is necessary to develop reliable biomarkers for epileptogenesis and cognitive impairment after traumatic brain injury when searching for novel antiepileptogenic and cognition-enhancing treatments. We hypothesized that a multiparametric magnetic resonance imaging (MRI) analysis along the septotemporal hippocampal axis could predict the development of post-traumatic epilepsy and cognitive impairment. We performed quantitative T2 and T2* MRIs at 2, 7 and 21 days, and diffusion tensor imaging at 7 and 21 days after lateral fluid-percussion injury in male rats. Morris water maze tests conducted between 35–39 days post-injury were used to diagnose cognitive impairment. One-month-long continuous video-electroencephalography monitoring during the 6th post-injury month was used to diagnose epilepsy. Single-parameter and regularized multiple linear regression models were able to differentiate between sham-operated and brain-injured rats. In the ipsilateral hippocampus, differentiation between the groups was achieved at most septotemporal locations (cross-validated area under the receiver operating characteristic curve (AUC) 1.0, 95% confidence interval 1.0–1.0). In the contralateral hippocampus, the highest differentiation was evident in the septal pole (AUC 0.92, 95% confidence interval 0.82–0.97). Logistic regression analysis of parameters imaged at 3.4 mm from the contralateral hippocampus’s temporal end differentiated between the cognitively impaired rats and normal rats (AUC 0.72, 95% confidence interval 0.55–0.84). Neither single nor multiparametric approaches could identify the rats that would develop post-traumatic epilepsy. Multiparametric MRI analysis of the hippocampus can be used to identify cognitive impairment after an experimental traumatic brain injury. This information can be used to select subjects for preclinical trials of cognition-improving interventions