We present what is to our knowledge the first reported case of thoracic disc herniation leading to venous congestive myelopathy (VCM), which was clinically and radiographically suggestive of Foix–Alajouanine syndrome (angiodysgenetic necrotizing myelopathy). In addition, we review current concepts in evaluating the etiology of VCM and discuss indications for surgery.
Foix–Alajouanine syndrome; spinal arteriovenous fistula; thoracic disc herniation; venous congestive myelopathy
Speech processing engages multiple cortical regions in the temporal, parietal, and frontal lobes. Isolating speech-sensitive cortex in individual participants is of major clinical and scientific importance. This task is complicated by the fact that responses to sensory and linguistic aspects of speech are tightly packed within the posterior superior temporal cortex. In functional magnetic resonance imaging (fMRI), various baseline conditions are typically used in order to isolate speech-specific from basic auditory responses. Using a short, continuous sampling paradigm, we show that reversed (“backward”) speech, a commonly used auditory baseline for speech processing, removes much of the speech responses in frontal and temporal language regions of adult individuals. On the other hand, signal correlated noise (SCN) serves as an effective baseline for removing primary auditory responses while maintaining strong signals in the same language regions. We show that the response to reversed speech in left inferior frontal gyrus decays significantly faster than the response to speech, thus suggesting that this response reflects bottom-up activation of speech analysis followed up by top-down attenuation once the signal is classified as nonspeech. The results overall favor SCN as an auditory baseline for speech processing.
fMRI; functional localizer; reversed speech; signal correlated noise; speech perception
In order to investigate whether or not prenatal and lactational exposure to bisphenol A (BPA) affects social behavior in mice, pregnant mice were exposed to 500 μg/kg of BPA daily from embryonic day 0 (E0) until postnatal day 21 (P21). The behavior of offspring was monitored at 11–13 and 13–15 weeks of age using an automated behavior assessment system (IntelliCage). Groups of eight mice were tasked with a nose poke, which enabled the mice to open a door to drink bottled water at the corner of their cage. BPA-exposed females visited the corner without drinking behavior during the light cycle less frequently than control female mice did. BPA-exposed males stayed at the corner for longer periods of time and showed a significantly stronger bias in the visit with drinking. In addition, the BPA-exposed males showed a shorter time interval before they visited the corner after preceding animals had visited it, compared with the control males. These findings suggest that prenatal and lactational BPA exposure might affect murine motivational behavior in a social setting differently in males and females.
Bisphenol A; development; IntelliCage; mice; social behavior
This study investigates the potential of independent component analysis (ICA) to provide a data-driven approach for group level analysis of magnetic resonance (MR) spectra. ICA collectively analyzes data to identify maximally independent components, each of which captures covarying resonances, including those from different metabolic sources. A comparative evaluation of the ICA approach with the more established LCModel method in analyzing two different noise-free, artifact-free, simulated data sets of known compositions is presented. The results from such ideal simulations demonstrate the ability of data-driven ICA to decompose data and accurately extract components resembling modeled basis spectra from both data sets, whereas the LCModel results suffer when the underlying model deviates from assumptions, thus highlighting the sensitivity of model-based approaches to modeling inaccuracies. Analyses with simulated data show that independent component weights are good estimates of concentrations, even of metabolites with low intensity singlet peaks, such as scyllo-inositol. ICA is also applied to single voxel spectra from 193 subjects, without correcting for baseline variations, line-width broadening or noise. The results provide evidence that, despite the presence of confounding artifacts, ICA can be used to analyze in vivo spectra and extract resonances of interest. ICA is a promising technique for decomposing MR spectral data into components resembling metabolite resonances, and therefore has the potential to provide a data-driven alternative to the use of metabolite concentrations derived from curve-fitting individual spectra in making group comparisons.
ICA; independent component analysis; LCModel; magnetic resonance spectroscopy; MR spectra decomposition; single voxel spectroscopy
Crucifixion as a means of torture and execution was first developed in the 6th century B.C. and remained popular for over 1000 years. Details of the practice, which claimed hundreds of thousands of lives, have intrigued scholars as historical records and archaeological findings from the era are limited. As a result, various aspects of crucifixion, including the type of crosses used, methods of securing victims to crosses, the length of time victims survived on the cross, and the exact mechanisms of death, remain topics of debate. One aspect of crucifixion not previously explored in detail is the characteristic hand posture often depicted in artistic renditions of crucifixion. In this posture, the hand is clenched in a peculiar and characteristic fashion: there is complete failure of flexion of the thumb and index finger with partial failure of flexion of the middle finger. Such a “crucified clench” is depicted across different cultures and from different eras. A review of crucifixion history and techniques, median nerve anatomy and function, and the historical artistic depiction of crucifixion was performed to support the hypothesis that the “crucified clench” results from proximal median neuropathy due to positioning on the cross, rather than from direct trauma of impalement of the hand or wrist.
Benediction sign; crucifixion; median nerve; neuropathy
Dopaminergic therapy in Parkinson's disease (PD) can improve some cognitive functions while worsening others. These opposite effects might reflect different levels of residual dopamine in distinct parts of the striatum, although the underlying mechanisms remain poorly understood. We used functional magnetic resonance imaging (fMRI) to address how apomorphine, a potent dopamine agonist, influences brain activity associated with working memory in PD patients with variable levels of nigrostriatal degeneration, as assessed via dopamine-transporter (DAT) scan. Twelve PD patients underwent two fMRI sessions (Off-, On-apomorphine) and one DAT-scan session. Twelve sex-, age-, and education-matched healthy controls underwent one fMRI session. The core fMRI analyses explored: (1) the main effect of group; (2) the main effect of treatment; and (3) linear and nonlinear interactions between treatment and DAT levels. Relative to controls, PD-Off patients showed greater activations within posterior attentional regions (e.g., precuneus). PD-On versus PD-Off patients displayed reduced left superior frontal gyrus activation and enhanced striatal activation during working-memory task. The relation between DAT levels and striatal responses to apomorphine followed an inverted-U-shaped model (i.e., the apomorphine effect on striatal activity in PD patients with intermediate DAT levels was opposite to that observed in PD patients with higher and lower DAT levels). Previous research in PD demonstrated that the nigrostriatal degeneration (tracked via DAT scan) is associated with inverted-U-shaped rearrangements of postsynaptic D2-receptors sensitivity. Hence, it can be hypothesized that individual differences in DAT levels drove striatal responses to apomorphine via D2-receptor-mediated mechanisms.
Cognition; DAT; dopamine-agonist; fMRI; Parkinson's disease; working memory
The ability to process facial expressions can be modified by altering the spatial frequency of the stimuli, an effect that has been attributed to differential properties of visual pathways that convey different types of information to distinct brain regions at different speeds. While this effect suggests a potential influence of spatial frequency on the processing speed of facial emotion, this hypothesis has not been examined directly. We addressed this question using a facial emotion identification task with photographs containing either high spatial frequency (HSF), low spatial frequency (LSF), or broadband spatial frequency (BSF). Temporal processing of emotion perception was manipulated by suppressing visual perception with a single-pulse transcranial magnetic stimulation (TMS), delivered to the visual cortex at six intervals prior to (forward masking) or following (backward masking) stimulus presentation. Participants performed best in the BSF, followed by LSF, and finally HSF condition. A spatial frequency by forward/backward masking interaction effect demonstrated reduced performance in the forward masking component in the BSF condition and a reversed performance pattern in the HSF condition, with no significant differences between forward and backward masking in the LSF condition. Results indicate that LSF information may play a greater role than HSF information in emotional processing, but may not be sufficient for fast conscious perception of emotion. As both LSF and HSF filtering reduced the speed of extracting emotional information from faces, it is possible that intact BSF faces have an inherent perceptual advantage and hence benefit from faster temporal processing.
Affect perception; facial emotion; transcranial magnetic stimulation; visual masking
The majority of neuroimaging studies focus on brain activity during performance of cognitive tasks; however, some studies focus on brain areas that activate in the absence of a task. Despite the surge of research comparing these contrasted areas of brain function, their interrelation is not well understood. We systematically manipulated cognitive load in a working memory task to examine concurrently the relation between activity elicited by the task versus activity during control conditions. We presented adults with six levels of task demand, and compared those with three conditions without a task. Using whole-brain analysis, we found positive linear relations between cortical activity and task difficulty in areas including middle frontal gyrus and dorsal cingulate; negative linear relations were found in medial frontal gyrus and posterior cingulate. These findings demonstrated balancing of activation patterns between two mental processes, which were both modulated by task difficulty. Frontal areas followed a graded pattern more closely than other regions. These data also showed that working memory has limited capacity in adults: an upper bound of seven items and a lower bound of four items. Overall, working memory and default-mode processes, when studied concurrently, reveal mutually competing activation patterns.
Default mode; difficulty; fMRI; working memory
Several studies have suggested the involvement of the hippocampus in the elaboration of epilepsy. There is evidence that suggests the hippocampus plays an important role in the affective and motivational components of nociceptive perception. However, the exact nature of this involvement remains unclear. Therefore, the aim of this study was to determine the role of muscarinic and nicotinic cholinergic receptors in the dorsal hippocampus (dH) in the organization of postictal analgesia. In a neuroanatomical study, afferent connections were found from the somatosensory cortex, the medial septal area, the lateral septal area, the diagonal band of Broca, and the dentate gyrus to the dH; all these areas have been suggested to modulate convulsive activity. Outputs to the dH were also identified from the linear raphe nucleus, the median raphe nucleus (MdRN), the dorsal raphe nucleus, and the locus coeruleus. All these structures comprise the endogenous pain modulatory system and may be involved either in postictal pronociception or antinociception that is commonly reported by epileptic patients. dH-pretreatment with cobalt chloride (1.0 mmol/L CoCl2/0.2 μL) to transiently inhibit local synapses decreased postictal analgesia 10 min after the end of seizures. Pretreatment of the dH with either atropine or mecamylamine (1.0 μg/0.2 μL) attenuated the postictal antinociception 30 min after seizures, while the higher dose (5.0 μg/0.2 μL) decreased postictal analgesia immediately after the end of seizures. These findings suggest that the dH exerts a critical role in the organization of postictal analgesia and that muscarinic and nicotinic cholinergic receptor-mediated mechanisms in the dH are involved in the elaboration of antinociceptive processes induced by generalized tonic-clonic seizures.
cholinergic neurotransmission; dorsal hippocampus; GABAergic neurotransmission; postictal analgesia
Earlier we demonstrated that the injection of neural progenitor cells (NPCs) has therapeutic potential for the improvement of learning dysfunction after cerebral ischemia. However, it remained to be clarified how transplantation of NPCs can improve ischemia-induced dysfunction. In this study, we examined whether intravenous injection of NPCs after cerebral ischemia could enhance angiogenesis by affecting the expression of angiogenic factors. The injection of NPCs on day 7 after cerebral ischemia enhanced angiogenesis on day 28. Vascular endothelial growth factor (VEGF) and its receptor VEGFR2 were increased in expression by the NPC injection. The level of angiopoietin-1 (Ang-1), an angiogenic factor, but not that of Ang-2, which acts as an antagonist for the Ang-1 receptor, was also increased on day 28. In addition, the expression of Ang-1 receptor Tie2 was enhanced in brain capillaries. Furthermore, the amounts of tight junctional proteins, which are in the blood–brain barrier and whose expression occurs downstream of Ang-1/Tie2 signaling, were increased by the NPC injection. These results suggest that the NPC injection promoted angiogenesis through Ang-1/Tie2 and/or VEGF/VEGFR2 signaling in brain capillaries after cerebral ischemia. Such signaling might have the potential for causing vascular stabilization and maturation for a long period after cerebral ischemia.
Angiopoietin; cerebral ischemia; neural progenitor cells; tight junctional protein; VEGF
Although motor tasks at most times do not require much attention, there are findings that attention can alter neuronal activity not only in higher motor areas but also within the primary sensorimotor cortex. However, these findings are equivocal as attention effects were investigated only in either the dominant or the nondominant hand; attention was operationalized either as concentration (i.e., attention directed to motor task) or as distraction (i.e., attention directed away from motor task), the complexity of motor tasks varied and almost no left-handers were studied. Therefore, in this study, both right- and left-handers were investigated with an externally paced button press task in which subjects typed with the index finger of the dominant, nondominant, or both hands. We introduced four different attention levels: attention-modulation-free, distraction (counting backward), concentration on the moving finger, and divided concentration during bimanual movement. We found that distraction reduced neuronal activity in both contra- and ipsilateral primary sensorimotor cortex when the nondominant hand was tapping in both handedness groups. At the same time, distraction activated the dorsal frontoparietal attention network and deactivated the ventral default network. We conclude that difficulty and training status of both the motor and cognitive task, as well as usage of the dominant versus the nondominant hand, are crucial for the presence and magnitude of attention effects on sensorimotor cortex activity. In the case of a very simple button press task, attention modulation is seen for the nondominant hand under distraction and in both handedness groups.
Attention; distraction; dual task; finger tapping; functional MRI; hand area; motor task; primary motor cortex
The combination of memantine, an N-methyl-d-aspartate (NMDA) receptor antagonist, with an acetylcholinesterase inhibitor (AChEI) is the current standard of care in Alzheimer's disease (AD). Galantamine, an AChEI currently marketed for the treatment of AD, exerts memory-enhancing and neuroprotective effects via activation of nicotinic acetylcholine receptors (nAChRs). Here, we investigated the neuroprotective properties of galantamine in primary cultures of rat cortical neurons when given alone or in combination with memantine. In agreement with previous findings, we found that memantine was fully effective in reversing NMDA toxicity at concentrations of 2.5 and 5 μmol/L. Galantamine also completely reversed NMDA toxicity at a concentration of 5 μmol/L. The α7 and α4β2 nAChR antagonists, methyllycaconitine, and dihydro-β-erythroidine blocked the neuroprotective effect of galantamine, demonstrating the involvement of nAChRs. The combination of memantine with galantamine produced synergistic actions, such that full neuroprotective efficacy, was obtained at inactive concentrations of memantine (0.1 μmol/L) and galantamine (1 μmol/L). A similar potentiation was also observed when memantine was replaced with ifenprodil, suggesting a possible involvement of the NR2B subunit of the NMDA receptor. In summary, our study reports for the first time at a cellular level that memantine and galantamine interact on the same excitotoxic cascade and that the combination of these two drugs can result in a remarkable neuroprotective effect.
Alzheimer's disease; drug combination; NMDA neurotoxicity; NR2B; polypharmacology; primary cortical neurons
Cerebral dopamine neurotrophic factor (CDNF) protein has been shown to protect the nigrostriatal dopaminergic pathway when given as intrastriatal infusions in rat and mouse models of Parkinson's disease (PD). In this study, we assessed the neuroprotective effect of CDNF delivered with a recombinant adeno-associated viral (AAV) serotype 2 vector in a rat 6-hydroxydopamine (6-OHDA) model of PD. AAV2 vectors encoding CDNF, glial cell line–derived neurotrophic factor (GDNF), or green fluorescent protein were injected into the rat striatum. Protein expression analysis showed that our AAV2 vector efficiently delivered the neurotrophic factor genes into the brain and gave rise to a long-lasting expression of the proteins. Two weeks after AAV2 vector injection, 6-OHDA was injected into the rat striatum, creating a progressive degeneration of the nigrostriatal dopaminergic system. Treatment with AAV2-CDNF resulted in a marked decrease in amphetamine-induced ipsilateral rotations while it provided only partial protection of tyrosine hydroxylase (TH)-immunoreactive cells in the rat substantia nigra pars compacta and TH-reactive fibers in the striatum. Results from this study provide additional evidence that CDNF can be considered a potential treatment of Parkinson's disease.
6-OHDA; AAV; CDNF; GDNF; gene therapy
The lack of reliable outcome predictors and the delayed onset of therapeutic response to antidepressants are among the clinical challenges in the treatment of depression. Identifying clinical correlates associated with antidepressant response would reduce symptom severity and morbidity for patients with depression. Twenty-three subjects with major depression were treated with citalopram 20 mg/day in a 6-week open trial and were also simultaneously randomized to either adjunctive triiodothyronine (T3) 25 μg BID (n = 7), pindolol 5 mg BID (n = 8), or placebo (n = 8). Baseline thyroid-stimulating hormone (TSH), FT4, FT3, and TT3 were measured for potential relationships to treatment response across groups. In males only, there was a significant inverse correlation between baseline free T4 and time to response (r = −0.7, P = 0.034). In both males and females across all treatment conditions, as measured by Kaplan–Meier (K–M) maintenance failure time, baseline TSH below the mean (1.5 ng/dL) was associated with a shorter time to response (50% reduction in Montgomery and Asberg Depression Rating Scale [MADRS] score) (χ2 = 4.53, df = 1, P = 0.03). Patients with baseline TSH above the mean were less likely to reach full remission (MADRS ≤ 7) (χ2 = 4.38, df = 1, P = 0.03). No significant differences between groups emerged in the mean response time. Baseline thyroid function, as measured by serum free T4 and TSH, may predict a patient's response time to antidepressant treatment with citalopram.
Acceleration; antidepressant response; citalopram; free thyroxine; thyroid; thyroid-stimulating hormone; triiodothyronine
By definition, patients with unresponsive wakefulness syndrome (UWS) do not experience pain, but it is still not completely understood how far their brain can process noxious stimuli. The few positron emission tomography studies that have examined pain processing did not yield a clear and consistent result. We performed an functional magnetic resonance imaging scan in 30 UWS patients of nontraumatic etiology and 15 age- and sex-matched healthy control participants (HC). In a block design, noxious electrical stimuli were presented at the patients' left index finger, alternating with a resting baseline condition. Sixteen of the UWS patients (53%) showed neural activation in at least one subsystem of the pain-processing network. More specifically, 15 UWS patients (50%) showed responses in the sensory-discriminative pain network, 30% in the affective pain network. The data indicate that some patients completely fulfilling the clinical UWS criteria have the neural substrates of noxious stimulation processing, which resemble that in control individuals. We therefore suppose that at least some of these patients can experience pain.
Functional magnetic resonance imaging; pain; unresponsive wakefulness syndrome
γ-Aminobutyric acid type A (GABAA) receptor plasticity participates in mediating adaptation to environmental change. Previous studies in rats demonstrated that extrasynaptic GABAA receptor subunits and receptors in the pons, a brainstem region involved in respiratory control, are upregulated by exposure to sustained hypobaric hypoxia. In these animals, expression of the mRNA encoding the extrasynaptic α4 subunit rose after 3 days in sustained hypoxia, while those encoding the α6 and δ subunits increased dramatically by 2 weeks. However, the participation of extrasynaptic subunits in maintaining respiration in normoxic conditions remains unknown. To examine the importance of α4 in a normal environment, respiratory function, motor and anxiety-like behaviors, and expression of other GABAA receptor subunit mRNAs were compared in wild-type (WT) and α4 subunit-deficient mice. Loss of the α4 subunit did not impact frequency, but did lead to reduced ventilatory pattern variability. In addition, mice lacking the subunit exhibited increased anxiety-like behavior. Finally, α4 subunit loss resulted in reduced expression of other extrasynaptic (α6 and δ) subunit mRNAs in the pons without altering those encoding the most prominent synaptic subunits. These findings on subunit-deficient mice maintained in normoxia, in conjunction with earlier findings on animals maintained in chronic hypoxia, suggest that the expression and regulation of extrasynaptic GABAA receptor subunits in the pons is interdependent and that their levels influence respiratory control as well as adaptation to stress.
Control of breathing; GABAA receptor subunits; pons; ventilatory response
Astrocytes are critical for maintaining homeostasis in the central nervous system (CNS), and also participate in the genomic response of the brain to drugs of abuse, including alcohol. In this study, we investigated ethanol regulation of gene expression in astrocytes. A microarray screen revealed that a brief exposure of cortical astrocytes to ethanol increased the expression of a large number of genes. Among the alcohol-responsive genes (ARGs) are glial-specific immune response genes, as well as genes involved in the regulation of transcription, cell proliferation, and differentiation, and genes of the cytoskeleton and extracellular matrix. Genes involved in metabolism were also upregulated by alcohol exposure, including genes associated with oxidoreductase activity, insulin-like growth factor signaling, acetyl-CoA, and lipid metabolism. Previous microarray studies performed on ethanol-treated hepatocyte cultures and mouse liver tissue revealed the induction of almost identical classes of genes to those identified in our microarray experiments, suggesting that alcohol induces similar signaling mechanisms in the brain and liver. We found that acute ethanol exposure activated heat shock factor 1 (HSF1) in astrocytes, as demonstrated by the translocation of this transcription factor to the nucleus and the induction of a family of known HSF1-dependent genes, the heat shock proteins (Hsps). Transfection of a constitutively transcriptionally active Hsf1 construct into astrocytes induced many of the ARGs identified in our microarray study supporting the hypothesis that HSF1 transcriptional activity, as part of the heat shock cascade, may mediate the ethanol induction of these genes. These data indicate that acute ethanol exposure alters gene expression in astrocytes, in part via the activation of HSF1 and the heat shock cascade.
Alcohol; alcohol response element; astrocytes; gene expression; glia; heat shock factor 1; microarray
Neuronal glucose uptake was thought to be independent of insulin, being facilitated by glucose transporters GLUT1 and GLUT3, which do not require insulin signaling. However, it is now known that components of the insulin-mediated glucose uptake pathway, including neuronal insulin synthesis and the insulin-dependent glucose transporter GLUT4, are present in brain tissue, particularly in the hippocampus. There is considerable recent evidence that insulin signaling is crucial to optimal hippocampal function. The physiological basis, however, is not clear. We propose that while noninsulin-dependent GLUT1 and GLUT3 transport is adequate for resting needs, the surge in energy use during sustained cognitive activity requires the additional induction of insulin-signaled GLUT4 transport. We studied hippocampal high-energy phosphate metabolism in eight healthy volunteers, using a lipid infusion protocol to inhibit insulin signaling. Contrary to conventional wisdom, it is now known that free fatty acids do cross the blood–brain barrier in significant amounts. Energy metabolism within the hippocampus was assessed during standardized cognitive activity. 31Phosphorus magnetic resonance spectroscopy was used to determine the phosphocreatine (PCr)-to-adenosine triphosphate (ATP) ratio. This ratio reflects cellular energy production in relation to concurrent cellular energy expenditure. With lipid infusion, the ratio was significantly reduced during cognitive activity (PCr/ATP 1.0 ± 0.4 compared with 1.4 ± 0.4 before infusion, P = 0.01). Without lipid infusion, there was no reduction in the ratio during cognitive activity (PCr/ATP 1.5 ± 0.3 compared with 1.4 ± 0.4, P = 0.57). This provides supporting evidence for a physiological role for insulin signaling in facilitating increased neuronal glucose uptake during sustained cognitive activity. Loss of this response, as may occur in type 2 diabetes, would lead to insufficient neuronal energy availability during cognitive activity.
Brain glucose uptake; diabetes; insulin signaling; neurometabolic coupling
Sporadic and familiar amyotrophic lateral sclerosis (ALS) cases presented lower cholinergic activity than in healthy individuals in their still preserved spinal motoneurons (MNs) suggesting that cholinergic reduction might occur before MN death. To unravel how and when cholinergic function is compromised, we have analyzed the spatiotemporal expression of choline acetyltransferase (ChAT) from early presymptomatic stages of the SOD1G93A ALS mouse model by confocal immunohistochemistry. The analysis showed an early reduction in ChAT content in soma and presynaptic boutons apposed onto MNs (to 76%) as well as in cholinergic interneurons in the lumbar spinal cord of the 30-day-old SOD1G93A mice. Cholinergic synaptic stripping occurred simultaneously to the presence of abundant surrounding major histocompatibility complex II (MHC-II)-positive microglia and the accumulation of nuclear Tdp-43 and the appearance of mild oxidative stress within MNs. Besides, there was a loss of neuronal MHC-I expression, which is necessary for balanced synaptic stripping after axotomy. These events occurred before the selective raise of markers of denervation such as ATF3. By the same time, alterations in postsynaptic cholinergic-related structures were also revealed with a loss of the presence of sigma-1 receptor, a Ca2+ buffering chaperone in the postsynaptic cisternae. By 2 months of age, ChAT seemed to accumulate in the soma of MNs, and thus efferences toward Renshaw interneurons were drastically diminished. In conclusion, cholinergic dysfunction in the local circuitry of the spinal cord may be one of the earliest events in ALS etiopathogenesis.
Amyotrophic lateral sclerosis; ChAT; MHC-I; motoneuron; presynaptic boutons; Tdp-43
Items that are distinctive with respect to their context tend to be recalled better than nondistinctive items, a finding known as the von Restorff effect. The goal of this study was to elucidate the role of novelty in this effect. In two experiments, participants performed a dual task in which they had to study words presented visually while to-be ignored sounds were played over earphones. Sounds could be either standard or novel, and words could be presented in standard or novel font. Sounds were presented either simultaneously with the words (Experiment 1) or preceding them (Experiment 2). Electrophysiological correlates of novelty processing, the N2b and P3a ERP components, were recorded while the words were studied. It was seen that cued recall was better for words presented in novel fonts than for words in a standard font (the von Restorff effect). Words presented while novel sounds were played were remembered worse (Experiment 1) or equally well (Experiment 2) than those combined with standard sounds. Words presented in novel fonts elicited enhanced N2b, P3a, P3b, and N400 components; however, none of these components were specifically larger for subsequently recalled novel-font words. A larger N2b was found for recalled than for nonrecalled words, but this effect was not specific for words presented in novel font. We hypothesized that if novelty was beneficial for memory processing, the N2–P3 complex would be more enhanced for novel words that were later recalled than for those not recalled. The data showed otherwise. This suggests that novelty processing, as indexed by the N2–P3 novelty components, is not the main cause of the von Restorff effect.
ERPs; N2; novelty; P3; von Restorff effect
Pineal gland and its hormone melatonin have been implicated in modulation of cardiovascular system. We aimed at studying the effects of melatonin on baroreflex sensitivity and the role of area postrema, as a component modulator of baroreflex arch. Mean arterial pressure (MAP) and heart rate (HR) were recorded in conscious freely moving rats. Baroreceptor reflex sensitivity was assessed by determining the HR responses to ramped infusions of phenylephrine (PE) and sodium nitroprusside (SNP)-induced MAP changes. Melatonin bolus (0.11 mg/kg) immediately followed by its continuous infusion (0.43 × 10−9 mol/L at a rate of 0.65 mL/h for 30 min) in healthy normotensive rats produced a downward shift of baroreceptor reflex control with a substantial inhibition of reflex tachycardia (−32%) and potentiation of reflex bradycardia (+20%). Ablation of area postrema (APX group) induced a sustained decrease of MAP (101 ± 3 vs. 116 ± 3 mmHg, P < 0.05 in comparison with sham rats, respectively). The melatonin-induced alterations of baroreflex function observed in the sham group were abolished in the APX group. We conclude that circulating melatonin can modulate baroreceptor reflex control of HR, thus resetting it toward lower HR values. The modulatory effects of melatonin may be mediated via melatonin receptors in the area postrema, located outside the blood–brain barrier.
Area postrema; baroreflex; blood pressure; heart rate; melatonin
The detailed time courses of cortical activities and source localizations following passive finger movement were studied using whole-head magnetoencephalography (MEG). We recorded motor-related cortical magnetic fields following voluntary movement and somatosensory-evoked magnetic fields following passive movement (PM) in 13 volunteers. The most prominent movement-evoked magnetic field (MEF1) following active movement was obtained approximately 35.3 ± 8.4 msec after movement onset, and the equivalent current dipole (ECD) was estimated to be in the primary motor cortex (Brodmann area 4). Two peaks of MEG response associated with PM were recorded from 30 to 100 msec after movement onset. The earliest component (PM1) peaked at 36.2 ± 8.2 msec, and the second component (PM2) peaked at 86.1 ± 12.1 msec after movement onset. The peak latency and ECD localization of PM1, estimated to be in area 4, were the same as those of the most prominent MEF following active movement. ECDs of PM2 were estimated to be not only in area 4 but also in the supplementary motor area (SMA) and the posterior parietal cortex (PPC) over the hemisphere contralateral to the movement, and in the secondary somatosensory cortex (S2) of both hemispheres. The peak latency of each source activity was obtained at 54–109 msec in SMA, 64–114 msec in PPC, and 84–184 msec in the S2. Our results suggest that the magnetic waveforms at middle latency (50–100 msec) after PM are different from those after active movement and that these waveforms are generated by the activities of several cortical areas, that is, area 4 and SMA, PPC, and S2. In this study, the time courses of the activities in SMA, PPC, and S2 accompanying PM in humans were successfully recorded using MEG with a multiple dipole analysis system.
Magnetoencephalography; MEF1; MEG; MRCF; PPC; S2; SEF; SMA
Disturbances of neural oscillation patterns have been reported with many disease states. We introduce methodology for HIRREM™ (high-resolution, relational, resonance-based electroencephalic mirroring), also known as Brainwave Optimization™, a noninvasive technology to facilitate relaxation and auto-calibration of neural oscillations. HIRREM is a precision-guided technology for allostatic therapeutics, intended to help the brain calibrate its own functional set points to optimize fitness. HIRREM technology collects electroencephalic data through two-channel recordings and delivers a series of audible musical tones in near real time. Choices of tone pitch and timing are made by mathematical algorithms, principally informed by the dominant frequency in successive instants of time, to permit resonance between neural oscillatory frequencies and the musical tones. Relaxation of neural oscillations through HIRREM appears to permit auto-calibration toward greater hemispheric symmetry and more optimized proportionation of regional spectral power. To illustrate an application of HIRREM, we present data from a randomized clinical trial of HIRREM as an intervention for insomnia (n = 19). On average, there was reduction of right-dominant temporal lobe high-frequency (23–36 Hz) EEG asymmetry over the course of eight successive HIRREM sessions. There was a trend for correlation between reduction of right temporal lobe dominance and magnitude of insomnia symptom reduction. Disturbances of neural oscillation have implications for both neuropsychiatric health and downstream peripheral (somatic) physiology. The possibility of noninvasive optimization for neural oscillatory set points through HIRREM suggests potentially multitudinous roles for this technology. Research is currently ongoing to further explore its potential applications and mechanisms of action.
Allostasis; auto-calibration; biofeedback; electroencephalography; hemispheric asymmetry; HIRREM; insomnia; neural oscillation; relaxation; stochastic resonance
This case report describes the use of high-resolution magnetic resonance imaging (HRMRI) to visualize basilar artery atherosclerotic plaque in a patient with a pontine stroke. HRMRI with three-dimensional image acquisition was used to visualize plaque in several planes to localize arterial wall pathology. Fluid attenuated inversion recovery (FLAIR) sequences of the basilar artery showed wall thickening throughout the basilar artery wall and good contrast between the artery wall and cerebrospinal fluid.
Basilar artery; cerebral infarction; intracranial atherosclerosis; magnetic resonance imaging; plaque; pontine stroke
In classical conditioning, an alteration in response occurs when two stimuli are regularly paired in close succession. An area of particular research interest is classical conditioning with a chemical signal and visual and/or tactile stimuli as the unconditional stimuli, to test manipulative and motor behaviors in a learning paradigm. A classical learning task chamber was developed to examine learning trends in a sighted surface-dwelling crayfish, Procambarus clarkii, and in a blind cave-dwelling crayfish, Orconectes australis packardi. We examined whether learning is influenced by environmental factors and/or reliance on different primary sensory modalities. Crayfish were trained to manipulate a large, cumbersome cheliped through a small access point to obtain a food reward. In both species, acquisition of the learning task was rapid when they were in nonstressed conditions. The blind crayfish tested in low white light did not successfully complete the task, suggesting a stress response.
Cardiac; central nervous system; crustaceans; instrumental; respiratory