Amplitude Of Evoked Potentials Research Articles

Observing nociceptive detection thresholds and evoked potentials in diabetic patients with and without painful neuropathy

Aim: Diabetic polyneuropathy is the most described complication in patients with diabetes mellitus. A significant percentage of these patients experience disabling neuropathic pain (painful diabetic polyneuropathy). Small nerve fibers are primarily responsible for peripheral nociception, but objectively assessing its function is challenging. The primary objective of this study was to explore the task execution and outcomes of intra-epidermal electrical stimulation technique that combines nociceptive detection thresholds (NDT) and evoked potentials (EPs) in patients with diabetes. We compared the results of diabetic patients, both with and without painful diabetic polyneuropathy, with those of healthy controls to explore potential clinically relevant information. Methods: The NDT-EP method was applied to 38 patients with diabetes (18 with and 20 without chronic painful neuropathy) and 38 age- and sex-matched healthy controls. Individual mean NDTs, psychometric slopes, EP amplitudes, and the effect of the stimuli on EP amplitudes were analyzed and compared between groups using linear regression. Results: The findings revealed significantly lower detection rates, higher NDTs, and lower psychometric slopes in patients with painful diabetic polyneuropathy than in healthy controls. Both patient groups significantly exhibited lower mean EP amplitudes than healthy controls, which were not linked to pulse amplitudes but influenced by stimulus detection. Conclusions: This study showed altered NDT-EP outcomes in patients with painful diabetic polyneuropathy. Whereas the task execution, NDTs, and psychometric slopes may provide valuable insights into small fiber dysfunction, pulse amplitudes seemed not differently encoded in neurophysiological responses to intra-epidermal electrical stimulation near the detection threshold compared to controls. Future studies should investigate whether the altered NDT-EP outcomes could quantify small fiber dysfunction in patients with diabetes mellitus. We recommend further exploration of NDT-EP measures in other patient groups with nociceptive dysfunction.

Agerelated parameters of P300 auditory evoked potentials in elderly persons in the context of cognitive health: A study in the European North of Russia

Background. Setting of norms for the parameters of P300 cognitive auditory evoked potentials (EP) in elderly people with intact cognitive functions considering their residence in certain climatic and geographical regions is an urgent problem.The aim of the study. To determine age-related parameters of P300 cognitive auditory evoked potentials in elderly people aged 60–69 and 70–74 years, living in the European North of Russia (using the example of Arkhangelsk).Methods. The parameters of P300 auditory EP were determined in randomly selected urban residents in the age groups of 60–69 years (n = 284) and 70–74 years (n = 115) with normal scores on the Montreal Cognitive Assessment Scale (MoCA), without depression (according to Beck Depression Inventory), with preserved ability to work and/or social functions. We calculated the 5th–95th percentile values (P5– P95) of the P300 EP parameters and assessed the relationships of these parameters with socio-demographic characteristics, lifestyle and the results on the MoCA scale and Beck Depression Inventory.Results. Statistically significant differences in latency indicators of P300 EP were determined between groups of 60–69 and 70–74 years (P25–P90) in all studied brain regions (frontal, central). In the group of 60–69 years, the range of P25–P75 values of P300 EP latencies was 342.5–401 ms, in the group of 70–74 years – 358.5–443 ms. Age differences in P300 EP amplitudes were minimal with an interquartile range of 4–13 μV in the total sample. Participants who smoked had higher latency scores and lower amplitude scores; former smokers had higher latency scores compared to never-smokers.Conclusion. Latency above 400 ms at the age of 60–65 years and above 443 ms at 70–74 years can be considered as a criterion for reduced cognitive reserve and an increased risk of developing cognitive disorders in elderly people living in the European North of Russia.

The pathobiology of psychomotor slowing in psychosis: altered cortical excitability and connectivity.

Psychomotor slowing is a frequent symptom of schizophrenia. Short-interval intracortical inhibition assessed by transcranial magnetic stimulation demonstrated inhibitory dysfunction in schizophrenia. The inhibitory deficit results from additional noise during information processing in the motor system in psychosis. Here, we tested whether cortical inhibitory dysfunction was linked to psychomotor slowing and motor network alterations. In this cross-sectional study, we included 60 patients with schizophrenia and psychomotor slowing determined by the Salpêtrière Retardation Rating Scale, 23 patients without slowing and 40 healthy control participants. We acquired single and double-pulse transcranial magnetic stimulation effects from the left primary motor cortex, resting-state functional connectivity and diffusion imaging on the same day. Groups were compared on resting motor threshold, amplitude of the motor evoked potentials, as well as short-interval intracortical inhibition. Regression analyses calculated the association between motor evoked potential amplitudes or cortical inhibition with seed-based resting-state functional connectivity from the left primary motor cortex and fractional anisotropy at whole brain level and within major motor tracts. In patients with schizophrenia and psychomotor slowing, we observed lower amplitudes of motor evoked potentials, while the short-interval intracortical inhibition/motor evoked potentials amplitude ratio was higher than in healthy controls, suggesting lower cortical inhibition in these patients. Patients without slowing also had lower amplitudes of motor evoked potentials. Across the combined patient sample, cortical inhibition deficits were linked to more motor coordination impairments. In patients with schizophrenia and psychomotor slowing, lower amplitudes of motor evoked potentials were associated with lower fractional anisotropy in motor tracts. Moreover, resting-state functional connectivity between the primary motor cortex, the anterior cingulate cortex and the cerebellum increased with stronger cortical inhibition. In contrast, in healthy controls and patients without slowing, stronger cortical inhibition was linked to lower resting-state functional connectivity between the left primary motor cortex and premotor or parietal cortices. Psychomotor slowing in psychosis is linked to less cortical inhibition and aberrant functional connectivity of the primary motor cortex. Higher neural noise in the motor system may drive psychomotor slowing and thus may become a treatment target.

Somatosensory evoked potentials amplitude is enhanced after non-invasive brain stimulation in chronic ischemic stroke: Preliminary results from a randomised control trial

ObjectiveTo investigate the effects of transcranial electrical and magnetic non-invasive brain stimulation (NIBS) protocols on somatosensory evoked potential (SEP) in chronic ischemic stroke. Methods33 patients were randomly assigned to one of the four treatment groups of the transcranial direct current stimulation (tDCS) and/or repetitive transcranial magnetic stimulation (rTMS) protocol. SEP parameters were recorded before and after ten days of the treatment session. All the statistical analyses were carried out using SPSS version 19. ResultsIt was found that there is a statistically significant improvement in the N20-P22 mean amplitude after treatment sessions in all groups except the group where tDCS and rTMS groups were sham. On paired t-tests, the difference betweeen post and pre-stimulation SEP amplitudes for the real tDCS and real rTMS coupled group was 1.045 ± 0.732 (p value = 0.005). For sham tDCS+real rTMS group, 1.05 ± 0.96 (P = 0.04); for real tDCS+sham rTMS 0.543 ± 0.332 (P = 0.01) and for double sham stimulation, 0.204 ± 0.648 (P = 0.4) respectively ConclusionIn ischemic stroke patients, either or coupled true transcranial tDCS and rTMS was found to be safe and significantly enhanced the amplitude of cortical somatosensory potentials when combined with standard physiotherapy, in the interim analysis of an ongoing randomised controlled trial. Clinical Trial Registry of IndiaCTRI/2019/11/022009 SignificanceThe results of this research indicates the importance of RCTs in developing robust improved NIBS protocols coupled to physiotherapy to enhance the sensory-motor functional recovery following ischemic stroke.

What is the effect of benzodiazepines on deep brain activity? A study in pediatric patients with dystonia.

Benzodiazepines (BDZs) are commonly used to treat the symptoms of movement disorders; however, deep brain stimulation (DBS) has become a popular treatment for these disorders. Previous studies have investigated the effects of BDZ on cortical activity, no data are currently available on their effects on deep brain regions, nor on these regions' responses to DBS. How the BDZ affects the thalamus and basal ganglia in dystonia patients remains unknown. DBS recordings were performed in ventral oralis anterior/posterior (VoaVop), ventral intermediate (VIM) and ventral anterior (VA) thalamic subnuclei, as well as globus pallidus interna (GPi) and subthalamic nucleus (STN). Evoked potentials (EP) and frequency domain analysis were performed to determine the BDZ effect on neural activities compared to the control condition (off-BDZ). Three male pediatric patients with dystonia treated with BDZ and undergoing depth electrode evaluation for clinical targeting were recruited for the study. Stimulation was administered at 25 and 55 Hz frequencies and recordings were simultaneously gathered through pairs of externalized stereoelectroencephalography (sEEG) electrodes. EP amplitude and the effect of stimulation on the frequency spectrum of activity were compared at baseline and following clinical administration of BDZ. Frequency analysis showed consistent reductions in activity during BDZ treatment in all studied brain regions for all patients. Evoked potential (EP) analysis showed increased subthalamic nucleus (STN) EP amplitude and decreased ventral intermediate (VIM) and STN EP amplitude during BDZ treatment. BDZs reduce thalamic and basal ganglia activity in multiple regions and alter the efficacy of transmission between these regions. While the mechanism is unknown our results confirm the known widespread effects of this class of medications and identify specific areas within the motor system that are directly affected.

The PanGut-study: Evoked potentials following rectal balloon distention, a way of evaluating diabetic autonomic neuropathy in the gut?

AimThere is a lack of methods for investigating the autonomic nerves of the gastrointestinal tract. Our aim was to explore a novel test measuring visceral sensory evoked potentials (EPs) in response to rapid balloon distention in the rectum and compare it to established tests for diabetic neuropathy. MethodParticipants with longstanding type 2 diabetes, newly onset, untreated diabetes <1 year, and matched controls, were included. Tests included cardiovascular reflex tests, orthostatic blood pressure, electrical skin conductance assessment, sural nerve testing and monofilament test. The rectal balloon distention pressure at earliest sensation and threshold of unpleasantness were identified and used to elicit mechanical EPs. ResultsThe pressure at earliest sensation was higher in people with diabetes, 0.038 (0.012) bar vs. controls 0.030 (0.009) bar, p = 0.002, and in people with signs of peripheral neuropathy, 0.045 (0.014) bar, p < 0.01. Clinical correlations between EP amplitude and latency, and other tests were found. ConclusionsRectal hyposensitivity was associated with both longstanding and early diabetes, indicating enteric sensory dysfunction already in early stages of diabetes. Correlation analyses may indicate that central afferent processing is affected in parallel with peripheral neuronal function.

Nimodipine accelerates the restoration of functional hyperemia during spreading oligemia.

Spreading depolarization (SD) is assumed to be the pathophysiological correlate of migraine aura, leading to spreading depression of activity and a long-lasting vasoconstriction known as spreading oligemia. Furthermore, cerebrovascular reactivity is reversibly impaired after SD. Here, we explored the progressive restoration of impaired neurovascular coupling to somatosensory activation during spreading oligemia. Also, we evaluated whether nimodipine treatment accelerated the recovery of impaired neurovascular coupling after SD. Male, 4-9-month-old C57BL/6 mice (n=11) were anesthetized with isoflurane (1%-1.5%), and SD was triggered with KCl through a burr hole made at the caudal parietal bone. EEG and cerebral blood flow (CBF) were recorded minimally invasively with a silver ball electrode and transcranial laser-Doppler flowmetry, rostral to SD elicitation. The L-type voltage-gated Ca2+ channel blocker nimodipine was administered i.p. (10mg/kg). Whisker stimulation-related evoked potentials (EVPs) and functional hyperemia were assessed under isoflurane (0.1%)-medetomidine (0.1mg/kg i.p.) anesthesia before, and repeatedly after SD, at 15-min intervals for 75 minutes. Nimodipine accelerated the recovery of CBF from spreading oligemia (time to full recovery, 52 ± 13 vs. 70 ± 8min, nimodipine vs. control) and exhibited a tendency to shorten the duration of the SD-related EGG depression duration. The amplitudes of EVP and functional hyperemia were markedly reduced after SD, and progressively recovered over an hour post-SD. Nimodipine exerted no impact on EVP amplitude but consistently increased the absolute level of functional hyperemia from 20 min post-CSD (93 ± 11% vs. 66 ± 13%, nimodipine vs. control). A linear, positive correlation between EVP and functional hyperemia amplitude was skewed by nimodipine. In conclusion, nimodipine facilitated CBF restoration from spreading oligemia and the recovery of functional hyperemia post-SD, which were linked to a tendency of an accelerated return of spontaneous neural activity after SD. The use of nimodipine in migraine prophylaxis is suggested to be re-visited.

How is neuromuscular fatigability affected by perceived fatigue and disability in people with multiple sclerosis?

Whereas fatigue is recognized to be the main complaint of patients with multiple sclerosis (PwMS), its etiology, and particularly the role of resistance to fatigability and its interplay with disability level, remains unclear. The purposes of this review were to (i) clarify the relationship between fatigue/disability and neuromuscular performance in PwMS and (ii) review the corticospinal and muscular mechanisms of voluntary muscle contraction that are altered by multiple sclerosis, and how they may be influenced by disability level or fatigue. Neuromuscular function at rest and during exercise are more susceptible to impairement, due to deficits in voluntary activation, when the disability is greater. Fatigue level is related to resistance to fatigability but not to neuromuscular function at rest. Neurophysiological parameters related to signal transmission such as central motor conduction time, motor evoked potentials amplitude and latency are affected by disability and fatigue levels but their relative role in the impaired production of torque remain unclear. Nonetheless, cortical reorganization represents the most likely explanation for the heightened fatigability during exercise for highly fatigued and/or disabled PwMS. Further research is needed to decipher how the fatigue and disability could influence fatigability for an ecological task, especially at the corticospinal level.

Long Term Performance of a Bi-Directional Neural Interface for Deep Brain Stimulation and Recording.

Background: In prior reports, we described the design and initial performance of a fully implantable, bi-directional neural interface system for use in deep brain and other neurostimulation applications. Here we provide an update on the chronic, long-term neural sensing performance of the system using traditional 4-contact leads and extend those results to include directional 8-contact leads.Methods: Seven ovine subjects were implanted with deep brain stimulation (DBS) leads at different nodes within the Circuit of Papez: four with unilateral leads in the anterior nucleus of the thalamus and hippocampus; two with bilateral fornix leads, and one with bilateral hippocampal leads. The leads were connected to either an Activa PC+S® (Medtronic) or Percept PC°ledR (Medtronic) deep brain stimulation and recording device. Spontaneous local field potentials (LFPs), evoked potentials (EPs), LFP response to stimulation, and electrode impedances were monitored chronically for periods of up to five years in these subjects.Results: The morphology, amplitude, and latencies of chronic hippocampal EPs evoked by thalamic stimulation remained stable over the duration of the study. Similarly, LFPs showed consistent spectral peaks with expected variation in absolute magnitude dependent upon behavioral state and other factors, but no systematic degradation of signal quality over time. Electrode impedances remained within expected ranges with little variation following an initial stabilization period. Coupled neural activity between the two nodes within the Papez circuit could be observed in synchronized recordings up to 5 years post-implant. The magnitude of passive LFP power recorded from directional electrode segments was indicative of the contacts that produced the greatest stimulation-induced changes in LFP power within the Papez network.Conclusion: The implanted device performed as designed, providing the ability to chronically stimulate and record neural activity within this network for up to 5 years of follow-up.

The monoclonal CGRP-receptor blocking antibody erenumab has different effects on brainstem and cortical sensory-evoked responses.

It is unclear whether the electrophysiological effects of erenumab, a monoclonal antibody against the calcitonin gene-related peptide receptor, occur only at the periphery of the trigeminal system or centrally and at the cortical level. We prospectively enrolled 20 patients with migraine who had failed at least two preventative treatments. We measured the nociceptive blink reflex and non-noxious somatosensory evoked potentials in all participants. The area under the curve and habituation of the second polysynaptic nociceptive blink reflex component (R2) as well as the amplitude and habituation of somatosensory evoked potentials N20-P25 were measured. Electrophysiological data were collected at baseline (T0), 28 days (T1), and 56 days (T2) before each injection of erenumab (70 mg). Erenumab reduced the patients' mean monthly headache days, headache intensity, and acute medication intake considerably at T1 and T2 (all p < 0.05). The nociceptive blink reflex area under the curve was considerably lower at T1 and T2 than at baseline without changing the habituation slope. At T2, there was a significant increase in the delayed somatosensory evoked potentials amplitude reduction (habituation) but not in the initial cortical activation. Our findings showed that erenumab, in addition to its well-known peripheral effects, can induce central effects earlier in the brainstem and later in the cortex. We cannot rule out whether these results are due to a direct effect of erenumab on the central nervous system or an indirect effect secondary to peripheral drug modulation.

In vivo blue light illumination for optogenetic inhibition: effect on local temperature and excitability of the rat hippocampus

Objective. The blue light-activated inhibitory opsin, stGtACR2, is gaining prominence as a neuromodulatory tool due its ability to shunt-inhibit neurons and is being frequently used in in vivo experimentation. However, experiments involving stGtACR2 use longer durations of blue light pulses, which inadvertently heat up the local brain tissue and confound experimental results. Therefore, the heating effects of illumination parameters used for in vivo optogenetic inhibition must be evaluated. Approach. To assess blue light (473 nm)-induced heating of the brain, we used a computational model as well as direct temperature measurements using a fiber Bragg grating (FBG). The effects of different light power densities (LPDs) and pulse durations on evoked potentials (EP) recorded from dentate gyrus were assessed. For opsin-negative rats, LPDs between 127 and 636 mW mm−2 and pulse durations between 20 and 5120 ms were tested while for stGtACR2 expressing rats, LPD of 127 mW mm−2 and pulse durations between 20 and 640 ms were tested. Main results. Increasing LPDs and pulse durations logarithmically increased the peak temperature and significantly decreased the population spike (PS) amplitude and latencies of EPs. For a pulse duration of 5120 ms, the tissue temperature increased by 0.6 °C–3.4 °C. All tested LPDs decreased the PS amplitude in opsin-negative rats, but 127 mW mm−2 had comparatively minimal effects and a significant effect of increasing light pulse duration was seen from 320 ms and beyond. This corresponded with an average temperature increase of 0.2 °C–1.1 °C at the recorded site. Compared to opsin-negative rats, illumination in stGtACR2-expressing rats resulted in much greater inhibition of EPs. Significance. Our study demonstrates that light-induced heating of the brain can be accurately measured in vivo using FBG sensors. Such light-induced heating alone can affect neuronal excitability. Useful neuromodulation by the activation of stGtACR2 is still possible while minimizing thermal effects.

Combined Evaluation of Nociceptive Detection Thresholds and Evoked Potentials during Conditioned Pain Modulation: A Feasibility Study.

Deficient top-down inhibitory control via diffuse noxious inhibitory control (DNIC) is a mechanism known to be responsible for the maintenance and development in several chronic pain syndromes. Experimentally, DNIC is often induced by conditioned pain modulation (CPM) paradigms such as a Cold Pressor Test (CPT). Recently, a method called the NDT-EP method has been developed with the aim to evaluate the nociceptive function, which it does via simultaneous tracking of nociceptive detection thresholds (NDT) and evoked potentials (EP). It remains to be investigated whether we can evaluate DNIC via the NDT-EP method. In this study, we take the first step to investigate this by evaluating the feasibility to combine the NDT-EP method with a 7 minutes CPT. In total 20 participants of a wide age-range were measured before, during, and after a CPT. All except 1 participant were able to complete the protocol, and enough stimulus-response pairs could be obtained for psychophysical as well as electrophysiological evaluation. Preliminary analysis of the NDT's and EP's showed results in line with earlier research such as a higher threshold for nociceptive stimuli and a lower EP amplitudes. Several NDT's of mostly elderly people (59±16 years), however, exceeded the maximum applicable stimulus strength during (7/20) or after (9/20) CPT and consequently had to be excluded from the analysis. To what extent this is a consequence of the CPT or other factors such as strong habituation associated more with elderly people, is subject to further investigation. In conclusion, the results of this study show that with the present protocol, it is feasible to combine the NDT-EP method with a CPM paradigm in almost all subjects, but that the NDT data of mostly older subjects could not be properly analyzed. Further directions for research and improvements are outlined.

Image-based biophysical modeling predicts cortical potentials evoked with subthalamic deep brain stimulation

BackgroundSubthalamic deep brain stimulation (DBS) is an effective surgical treatment for Parkinson’s disease and continues to advance technologically with an enormous parameter space. As such, in-silico DBS modeling systems have become common tools for research and development, but their underlying methods have yet to be standardized and validated. ObjectiveEvaluate the accuracy of patient-specific estimates of neural pathway activations in the subthalamic region against intracranial, cortical evoked potential (EP) recordings. MethodsPathway activations were modeled in eleven patients using the latest advances in connectomic modeling of subthalamic DBS, focusing on the hyperdirect pathway (HDP) and corticospinal/bulbar tract (CSBT) for their relevance in human research studies. Correlations between pathway activations and respective EP amplitudes were quantified. ResultsGood model performance required accurate lead localization and image fusions, as well as appropriate selection of fiber diameter in the biophysical model. While optimal model parameters varied across patients, good performance could be achieved using a global set of parameters that explained 60% and 73% of electrophysiologic activations of CSBT and HDP, respectively. Moreover, restricted models fit to only EP amplitudes of eight standard (monopolar and bipolar) electrode configurations were able to extrapolate variation in EP amplitudes across other directional electrode configurations and stimulation parameters, with no significant reduction in model performance across the cohort. ConclusionsOur findings demonstrate that connectomic models of DBS with sufficient anatomical and electrical details can predict recruitment dynamics of white matter. These results will help to define connectomic modeling standards for preoperative surgical targeting and postoperative patient programming applications.

The Application of Regional Cerebral Oxygenation Monitoring in the Prediction of Cerebral Hypoperfusion During Carotid Endarterectomy.

The aim of this study was to assess the diagnostic ability of near-infrared spectroscopy-monitored regional cerebral oxygen saturation (rSO2) to detect cerebral hypoperfusion during internal carotid artery (ICA) clamping compared with motor and somatosensory evoked potential (EP) monitoring. This prospective study recruited consecutive patients undergoing carotid endarterectomy under general anesthesia. Significant EP changes (defined as >50% decrease in ipsilateral somatosensory EP amplitude or disappearance of contralateral motor EP on >2 consecutive stimulations) during ICA clamping were considered a warning sign for cerebral hypoperfusion. If significant EP changes occurred, the amplitude of the EPs and simultaneous rSO2 values were recorded before therapeutic intervention. The relationship between reductions in rSO2 and EP amplitudes was analyzed using Spearman rank-correlation analysis. Receiver operating characteristic curve analysis was used to calculate the optimal cutoff value for the relative reduction in rSO2. False-positive rates were evaluated according to immediate postoperative motor outcomes. A total of 203 patients were included for analysis, of whom 23 developed significant EP changes during ICA clamping. There was a positive relationship between decreases in EP amplitude and rSO2 (R2=0.15, P=0.02). A rSO2 reduction ≥16% from baseline had the optimal diagnostic performance for the detection of cerebral hypoperfusion (area under the receiver operating characteristic curve=0.82; 95% confidence interval: 0.76-0.87). The false-positive rate was 8.9%. Decreases in rSO2 correlated with decreases in EP amplitude during ICA clamping. A relative reduction in rSO2 ≥16% could serve as a warning for clamping-associated cerebral hypoperfusion. The 8.9% false-positive rate is a potential clinical limitation of the use of rSO2 to predict postoperative neurological deficits.

Added value of somato-sensory evoked potentials amplitude for prognostication after cardiac arrest

AimsBilateral absence of cortical somato-sensory evoked potentials (SSEPs) robustly predicts poor outcome after cardiac arrest (CA), but it is uncertain if SSEP amplitudes provide additional information. Here, we examined the prognostic value of cortical SSEP amplitude in comparison with other known outcome predictors. MethodsWe retrospectively determined SSEP amplitudes in a prospective CA registry, identified an amplitude cut-off for worst Cerebral Performance Category (CPC) within three months, and examined correlations of SSEP amplitude with pupillary light reflex (PLR), myoclonus, peak serum neuron specific enolase (NSE), and 24–36 h and 36–72 h EEG (reactivity, epileptiform features). ResultsAmong 158 patients, 54% awoke. Amplitudes correlated with EEG findings, present PLR, myoclonus, NSE. A cut-off for cortical SSEP ≤ 0.41 μV was 100% specific for poor outcome (95% CI: 96–100%); sensitivity increased marginally vs. SSEPs absence [47% (35–59%) vs 46% (34–58%)] for CPC 4–5. Adding SSEPs ≤0.41 μV to a multimodal prognostic model including EEG, clinical features, and NSE improved prediction for mortality, but not for CPC 3–5 at three months. No statistical correlation between amplitudes and good outcome was observed. SSEP amplitudes correlated inversely with CPC at three months in the overall cohort (r = −0.332; p < 0.0001) but not in the subgroup with present SSEPs (r = −0.102; p = 0.256). ConclusionDecreased SSEPs amplitudes are associated with poor outcome after cardiac arrest; however, adding this to a multimodal prognostic approach including EEG, clinical and blood biomarkers, improves slightly prediction of mortality, but not of poor or good outcome.

Enriched environment provides neuroprotection against experimental glaucoma.

Glaucoma is one of the most frequent causes of visual impairment worldwide, and involves selective damage to retinal ganglion cells (RGCs) and their axons. We analyzed the effect of enriched environment (EE) housing on the optic nerve, and retinal alterations in an induced model of ocular hypertension. For this purpose, male Wistar rats were weekly injected with vehicle or chondroitin sulfate (CS) into the eye anterior chamber for 10weeks and housed in standard environment or EE. EE housing prevented the effect of experimental glaucoma on visual evoked potentials, retinal anterograde transport, phosphorylated neurofilament-immunoreactivity, axon number, microglial/macrophage reactivity (ionized calcium binding adaptor molecule 1-immunoreactivity), and astrocytosis (glial fibrillary acidic protein-immunostaining), as well as oligodendrocytes alterations (luxol fast blue staining, and myelin basic protein-immunoreactivity) in the proximal portion of the optic nerve. Moreover EE prevented the increase in ionized calcium binding adaptor molecule-1 levels, and RGC loss (Brn3a-immunoreactivity) in the retina from hypertensive eyes. EE increased retinal brain-derived neurotrophic factor levels. When EE housing started after 6weeks of ocular hypertension, a preservation of visual evoked potentials amplitude, axon, and Brn3a(+) RGC number was observed. Taken together, these results suggest that EE preserved visual functions, reduced optic nerve axoglial alterations, and protected RGCs against glaucomatous damage.

Serial Visual Evoked Potentials in Patients with Craniosynostosis and Invasive Intracranial Pressure Monitoring.

This study aimed to detect the ability of pattern visual evoked potentials to detect visual pathway dysfunction in a cohort of patients with craniosynostosis who also had invasive intracranial pressure measurement. A retrospective review was conducted on craniosynostosis patients who had invasive intracranial pressure measurement and at least one pattern visual evoked potentials test. Reversal pattern visual evoked potentials were performed with both eyes open. Thirteen patients met the inclusion criteria (mean age at intracranial pressure measurement, 5.7 years). Seven patients had raised intracranial pressure, and of these, five (71.4 percent) had abnormal or deteriorated pattern visual evoked potentials parameters on serial testing, whereas all patients (100 percent) with normal intracranial pressure had normal pattern visual evoked potentials amplitude and latency. Four of the five patients (80 percent) with raised intracranial pressure and abnormal pattern visual evoked potentials did not show evidence of papilledema. The mean latency in patients with raised intracranial pressure (118.7 msec) was longer than in those with normal intracranial pressure (108.1 msec), although it did not reach statistical significance (p = 0.09), whereas the mean amplitude in patients with raised intracranial pressure (12.4 µV) was significantly lower than in patients with normal intracranial pressure (23.3 µV) (p = 0.03). The authors' results showed that serial pattern visual evoked potentials testing was able to detect visual pathway dysfunction resulting from raised intracranial pressure in five of seven craniosynostosis patients, and of these five patients, 80 percent had no evidence of papilledema, demonstrating the utility of serial pattern visual evoked potentials in follow-up of the visual function in craniosynostosis patients. CLINICAL QUESTION/LEVEL OF EVIDENCE:: Diagnostic, II.

O-06 Motor cortex excitability and conduction time of pyramidal tracts in preclinical SCA1 gene carriers

Background Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative, dominantly inherited disease caused by CAG repeat expansion. It manifests mainly as trunk and limbs ataxia, dysarthria, gaze palsy and peripheral neuropathy. We aimed to assess the functional alterations of corticospinal tracts in preclinical SCA1 gene carriers performed during 4-years follow-up. Methods Transcranial magnetic stimulation (TMS) was carried out in 26 SCA1 gene carries with age at study entry 25.6 ± 4.7, CAG repeat number 49.5 ± 4.8 and 30 age- and gender-matched healthy controls (HC). Presence of ataxia was assessed by the Scale for Assessment and Rating of Ataxia (SARA). TMS was performed every ± 12 months to evaluate motor threshold (MT), silent period (SP) from hypothenar and extensor digitorum brevis muscles, central motor conduction time (CMCT) and motor evoked potentials amplitude (MEPs). Results Baseline SARA score increased from 0.6 ± 0.7 to 4.9 ± 5.2 points across follow-up. In 43% SCA1 cases MT of lower limbs was elevated and MEPs were in 35% decreased. SP was longer (p Conclusions In the preclinical SCA1 gene carriers before the onset of overt clinical signs TMS revealed functional alterations of corticospinal pathways. TMS could serve as an objective measure of disease progression in SCA1 patients.

Length-dependent truncal Aδ-fiber dysfunction in hereditary transthyretin amyloidosis: An intra-epidermal electrical stimulation study

ObjectiveTo elucidate Aδ-fiber dysfunction at the trunk in patients with hereditary transthyretin (ATTRm) amyloidosis using intra-epidermal electrical stimulation (IES). MethodsIn 16 patients with ATTRm amyloidosis and 18 healthy subjects, sensory thresholds using IES and cooling detection thresholds using the Computer-Aided Sensory Evaluation (CASE IV) system, were assessed to investigate Aδ-fiber functions at the Th10 level of the anterior, lateral, and posterior trunk. Furthermore, evoked potentials (EPs) following electrical stimulation using IES at the anterior and posterior trunk were evaluated. ResultsIn patients with ATTRm amyloidosis, both IES and CASE IV sensory thresholds tended to be higher at the anterior trunk than at the lateral and posterior trunks. The amplitudes of EPs following electrical stimulation at the anterior trunk were lower than those at the posterior trunk. Aδ-fiber dysfunction at the anterior trunk was conspicuous in patients with more intense polyneuropathy at the limbs. In healthy subjects, there were no differences in both sensory thresholds and EP amplitudes among any examination sites. Sensory thresholds with IES and CASE IV were correlated. ConclusionsEvaluation using IES demonstrated length-dependent Aδ-fiber dysfunction at the trunk in patients with ATTRm amyloidosis. SignificanceIES may be a useful clinical tool for investigating Aδ-fiber dysfunction at various parts of the body in patients with neuropathy.

Intraoperative use of transcranial motor/sensory evoked potential monitoring in the clipping of intracranial aneurysms: evaluation of false-positive and false-negative cases.

Somatosensory and motor evoked potentials (SEPs and MEPs) are often used to prevent ischemic complications during aneurysm surgeries. However, surgeons often encounter cases with suspicious false-positive and false-negative results from intraoperative evoked potential (EP) monitoring, but the incidence and possible causes for these results are not well established. The aim of this study was to investigate the efficacy and reliability of EP monitoring in the microsurgical treatment of intracranial aneurysms by evaluating false-positive and false-negative cases. From January 2012 to April 2016, 1514 patients underwent surgery for unruptured intracranial aneurysms (UIAs) with EP monitoring at the authors' institution. An EP amplitude decrease of 50% or greater compared with the baseline amplitude was defined as a significant EP change. Correlations between immediate postoperative motor weakness and EP monitoring results were retrospectively reviewed. The authors calculated the sensitivity, specificity, and positive and negative predictive values of intraoperative MEP monitoring, as well as the incidence of false-positive and false-negative results. Eighteen (1.19%) of the 1514 patients had a symptomatic infarction, and 4 (0.26%) had a symptomatic hemorrhage. A total of 15 patients showed motor weakness, with the weakness detected on the immediate postoperative motor function test in 10 of these cases. Fifteen false-positive cases (0.99%) and 8 false-negative cases (0.53%) were reported. Therefore, MEP during UIA surgery resulted in a sensitivity of 0.10, specificity of 0.94, positive predictive value of 0.01, and negative predictive value of 0.99. Intraoperative EP monitoring has high specificity and negative predictive value. Both false-positive and false-negative findings were present. However, it is likely that a more meticulously designed protocol will make EP monitoring a better surrogate indicator of possible ischemic neurological deficits.