Electrophysiological Findings Research Articles

A cortical field theory - dynamics and symmetries.

We characterise cortical dynamics using partial differential equations (PDEs), analysing various connectivity patterns within the cortical sheet. This exploration yields diverse dynamics, encompassing wave equations and limit cycle activity. We presume balanced equations between excitatory and inhibitory neuronal units, reflecting the ubiquitous oscillatory patterns observed in electrophysiological measurements. Our derived dynamics comprise lowest-order wave equations (i.e., the Klein-Gordon model), limit cycle waves, higher-order PDE formulations, and transitions between limit cycles and near-zero states. Furthermore, we delve into the symmetries of the models using the Lagrangian formalism, distinguishing between continuous and discontinuous symmetries. These symmetries allow for mathematical expediency in the analysis of the model and could also be useful in studying the effect of symmetrical input from distributed cortical regions. Overall, our ability to derive multiple constraints on the fields - and predictions of the model - stems largely from the underlying assumption that the brain operates at a critical state. This assumption, in turn, drives the dynamics towards oscillatory or semi-conservative behaviour. Within this critical state, we can leverage results from the physics literature, which serve as analogues for neural fields, and implicit construct validity. Comparisons between our model predictions and electrophysiological findings from the literature - such as spectral power distribution across frequencies, wave propagation speed, epileptic seizure generation, and pattern formation over the cortical surface - demonstrate a close match. This study underscores the importance of utilizing symmetry preserving PDE formulations for further mechanistic insights into cortical activity.

Absolute beta power in exercisers and nonexercisers in preparation for the oddball task.

High levels of physical conditioning are associated with improvements in cognitive performance. In this sense, electroencephalographic (ECG) correlates are used to investigate the enhancing role of physical exercise on executive functions. Oscillations in the β frequency range are proposed to be evident during sensorimotor activity. To investigate the ECG changes influenced by aerobic and resistance exercises performed in an attention task by analyzing the differences in absolute β power in the prefrontal and frontal regions before, during, and after the oddball paradigm in practitioners and nonpractitioners of physical exercise. There were 15 physical activity practitioners (aged 27 ± 4.71) and 15 nonpractitioners (age 28 ± 1.50) recruited. A two-way analysis of variance (ANOVA) was implemented to observe the main effect and the interaction between groups and moments (rest 1, pre-stimulus, and rest 2). An interaction between group and moment factors was observed for Fp1 (p < 0.001); Fp2 (p = 0.001); F7 (p < 0.001); F8 (p < 0.001); F3 (p < 0.001); Fz (p < 0.001); and F4 (p < 0.001). Electrophysiological findings clarified exercisers' specificity and neural efficiency in each prefrontal and frontal subarea. Our findings lend support to the current understanding of the cognitive processes underlying physical exercise and provide new evidence on the relationship between exercise and cortical activity.

Microscopical anatomy of the peripheral nervous system: An essential notion for understanding the pathophysiology of very early classic Guillain-Barré syndrome.

The aim of this paper is to analyze the pathophysiological mechanisms acting in very early classic Guillain-Barré syndrome (GBS) (≤4 days of symptomatic onset). In this inaugural period, both in GBS and its animal model, experimental autoimmune neuritis, the outstanding pathological feature is inflammatory edema predominating in proximal nerve trunks, particularly spinal nerves, and possibly in preterminal nerve segments. Nerve trunks external to the subarachnoid angle possess epi- perineurium that is relatively inelastic and of low compliance. Here such edema can increase endoneurial fluid pressure that, when sufficiently critical, may stretch the perineurium and constrict transperineurial microcirculation, compromising blood flow and producing the potential for ischemic nerve injury, whose consequence is rapid partial or complete loss of nerve excitability. These histopathological features correlate well with electrophysiological and imaging findings reported in early GBS stages. Spinal nerve edema and ischemia help to understand the pattern of Wallerian-like degeneration observed in the axonal form of GBS, predominating in motor spinal roots at their exit from the dura matter (spinal nerves) with centrifugal distribution in more distant motor nerve trunks, and centripetal extension to the distal portion of intrathecal roots. The similarity of initial pathogenic mechanisms between demyelinating and axonal forms of GBS explains why an early increase of serum biomarkers of axonal damage is detected in both forms. In conclusion, knowledge of the microscopic anatomy of the peripheral nervous system is an essential step for a reliable understanding of pathophysiological mechanisms operating in the early phase of any classic GBS subtype.

DMXL2 Is Required for Endocytosis and Recycling of Synaptic Vesicles in Auditory Hair Cells.

Ribbon synapses of inner hair cells (IHCs) are uniquely designed for ultrafast and indefatigable neurotransmission of the sound. The molecular machinery ensuring the efficient, compensatory recycling of the synaptic vesicles (SVs), however, remains elusive. This study showed that hair cell knock-out of murine Dmxl2, whose human homolog is responsible for nonsyndromic sensorineural hearing loss DFNA71, resulted in auditory synaptopathy by impairing synaptic endocytosis and recycling. The mutant mice in the C57BL/6J background of either sex had mild hearing loss with severely diminished wave I amplitude of the auditory brainstem response. Membrane capacitance measurements of the IHCs revealed deficiency in sustained synaptic exocytosis and endocytic membrane retrieval. Consistent with the electrophysiological findings, 3D electron microscopy reconstruction showed reduced reserve pool of SVs and endocytic compartments, while the membrane-proximal and ribbon-associated vesicles remain intact. Our results propose an important role of DMXL2 in hair cell endocytosis and recycling of the SVs.

Context-dependent neural preparation for information relevance vs. probability

Abstract Preparation is a top-down phenomenon known to improve performance across different situations. In light of recent electrophysiological findings that suggest that anticipatory neural preactivations linked to preparation are context-specific and do not generalize across domains, in the current study we used fMRI to investigate the brain regions involved in these differential patterns. We applied multivariate decoding to data obtained in a paradigm where, in different blocks, cues provided information about the relevance or probability of incoming target stimuli. Results showed that the anticipated stimulus category was pre-activated in both conditions, mostly in different brain regions within the ventral visual cortex and with differential overlap with actual target perception. Crucially, there was scarce cross-classification across attention and expectation contexts except on a patch of the fusiform gyrus, indicating mostly differential neural coding of anticipated contents in relevance and probability scenarios. Finally, a model-based fMRI-EEG fusion showed that these regions differentially code for specific conditions during preparation, as well as specifically preparing for category anticipation in a ramping-up manner. Overall, our results stress the specificity of anticipatory neural processing depending on its informative role while highlighting a key hub of commonality in the fusiform gyrus.

ITPR3-associated neuropathy: Report of a further family with adult onset intermediate Charcot-Marie-Tooth disease.

ITPR3 encodes type 3 inositol-tri-phosphate receptor (IP3R3), a protein expressed in Schwann cells, predominantly in the paranodal region, and involved in the regulation of Ca2+ release from the endoplasmic reticulum. Dominant variants in ITPR3 have recently been recognized as a rare cause of intermediate Charcot-Marie-Tooth disease (CMT). We collected the clinical data of a family with autosomal dominant neuropathy whose proband was diagnosed with chronic inflammatory demyelinating polyneuropathy (CIDP) for many years. The genetic diagnosis was achieved by whole exome sequencing. The proband developed symmetrical sensory-motor neuropathy with demyelinating features at 32 years old. He was diagnosed with CIDP and received numerous immunomodulatory treatments. However, his condition progressed, leading to severe proximal leg and hand atrophy that confined him to a wheelchair at 60 years. The patient's two sons began to exhibit symptoms suggestive of neuropathy shortly after age 30 years, and the condition was reoriented as inherited. Exome sequencing identified a heterozygous c.4271C > T variant in the ITPR3 gene segregating with the disease. Nerve conduction studies showed a combination of demyelinating and axonal features that vary by nerve, disease duration, and patient. A uniform thickening of the nerves was identified on nerve echography, as was distal symmetric fatty infiltration in lower limb muscle imaging. The c.4271C > T ITPR3 variant causes a late onset CMT that can be considered an intermediate CMT. Considering the electrophysiological findings and the distribution of IP3R3, we hypothesize that this variant could start as nodal dysfunction that progresses to widespread nerve degeneration.

Guillain-Barrè Syndrome-Retrospective Analysis of Data from a Cohort of Patients Referred to a Tertiary Care Pediatric Neuromuscular Center from 2000 to 2017: Electrophysiological Findings, Outcomes, and a Brief Literature Review.

Background and Objectives: Guillain-Barré syndrome (GBS) is the most frequent cause of acute flaccid paresis in children. The aim of this study was to describe the clinical and electrophysiological findings and outcomes of children with GBS diagnosed in our unit. Moreover, the literature on pediatric GBS cases from the past 5 years was reviewed. In this retrospective study, we reported data on 12 patients (9 male and 3 female patients; mean age: 5 y, 4 mo; range: 9 mo-11 y) clinically diagnosed at the Child Neurology Unit of the AUSL-IRCCS of Reggio Emilia, Italy, between 2000 and 2017 and a brief analysis/comparison with data from the literature. Materials and Methods: Data were collected from medical charts. Results: In our cohort, male patients were more frequent than female ones (9 vs. 3), and upper respiratory tract infection (n = 8, 66.7%) was the most frequent triggering factor. The main clinical symptoms on admission were distal lower limbs' weakness with gait difficulties (83.3%), pain (50%), upper limbs' weakness (50%), and dysphagia for liquids (25%). Peripheral neurophysiological studies revealed acute inflammatory demyelinating polyradiculoneuropathy (AIDP) in 66.6% of the children, acute motor and sensory axonal neuropathy (AMSAN) in 25%, and acute motor axonal neuropathy (AMAN) in 8.3%. Ten individuals (83.3%) received timely treatment with intravenous immunoglobulins (IVIG), and, out of these ten patients, 58% received concomitant treatment with IV methylprednisolone because of a progressive disease course. Complete remission was observed in the majority of individuals (91.6%) within 6 months of symptom onset. Conclusions: Different subtypes of GBS can affect children; however, the outcome is usually positive. Early treatment appears to be important for a favorable outcome.

Isaacs’ syndrome: Clinical and paraclinical perspectives in a series of cases

Background: Isaacs’ syndrome is a form of generalized peripheral nerve hyperexcitability (PNH) causing increased and continuous muscle activity characterized by muscle twitching, stiffness, cramps, myokymia, and pseudomyotonia. Herein, we aimed to review the clinical and paraclinical aspects of Isaacs’ syndrome in a number of cases. Methods: We reported a series of 12 patients with Isaacs’ syndrome, including their clinical features, electrophysiological findings, laboratory parameters, malignancy work-up, and therapeutic management. Results: In all cases, clinical and electrodiagnostic assessment was suggestive of Isaacs’ syndrome. Of the 12 studied cases, 5 patients were positive for both leucine-rich glioma inactivated 1 (LGI1) and contactin-associated protein-like 2 (CASPR2) antibodies, 5 patients were CASPR2 positive and LGI1 negative, and 1 had borderline positive titers for CASPR2 with negative LGI1 antibody. The search for underlying malignancies was inconclusive in all subjects. After symptomatic treatment, mostly with carbamazepine or gabapentin, immunotherapies with double filtration plasmapheresis or Intravenous immunoglobulin (IVIG) provided favorable outcomes. Ultimately, all subjects fully recovered after 3-6 months of follow-up and all signs and symptoms resolved. Conclusion: Despite the rarity of the disease, our results provide valuable information for understanding the epidemiological, clinical, and paraclinical features of Isaacs’ syndrome.

Behavioral regression in shank3Δex4-22 mice during early adulthood corresponds to cerebellar granule cell glutamatergic synaptic changes.

Shank3, a gene encoding a synaptic scaffolding protein, is implicated in autism spectrum disorder (ASD) and is disrupted in Phelan-McDermid syndrome (PMS). Despite evidence of regression or worsening of ASD-like symptoms in individuals with PMS, the underlying mechanisms remain unclear. Although shank3 is highly expressed in the cerebellar cortical granule cells, its role in cerebellar function and contribution to behavioral deficits in ASD models are unknown. This study investigates behavioral changes and cerebellar synaptic alterations in shank3Δex4-22 mice at two developmental stages. Shank3Δex4-22 wildtype, heterozygous, and homozygous knockout mice lacking exons 4-22 (all functional isoforms) were subjected to a behavioral battery in both juvenile (5-7 weeks old) and adult (3-5 months old) mouse cohorts of both sexes. Immunostaining was used to show the expression of SHANK3 in the cerebellar cortex. Spontaneous excitatory postsynaptic currents (sEPSCs) from cerebellar granule cells (CGCs) were recorded by whole-cell patch-clamp electrophysiology. Deletion of shank3ex4-22 caused deficits in motor function, heightened anxiety, and repetitive behaviors. These genotype-dependent behavioral alterations were more prominent in adult mice than in juveniles. Reduced social preference was only identified in adult shank3Δex4-22 knockout mice and self-grooming was uniquely elevated only in males across both age groups. Immunofluorescence staining indicates the presence of SHANK3 predominantly in the dendrite-containing rosette-like structures in CGCs, colocalizing with presynaptic markers of glutamatergic mossy fiber. Electrophysiological findings identify a parallel relationship between the age-related exacerbation of behavioral impairments and the enhancement of sEPSC amplitude in CGCs. Other behavioral tests of muscle strength (grip strength test), memory (Barnes/water maze), and communication (ultrasonic vocalization), were not performed. Further study is necessary to elucidate how SHANK3 modulates synaptic function at the mossy fiber-granule cell synapse in the cerebellum. Our findings reveal an age-related exacerbation of behavioral impairments in shank3Δex4-22 mutant mice. These results suggest that SHANK3 may play a role in maintaining glutamatergic receptors and synapses in CGCs, as well as the potential involvement of the cerebellum in ASD.

A revisit to interactions of stimulus quality and semantic context on N400 in visual word recognition.

Much behavioral research has revealed interactive effects between stimulus quality and semantic priming in visual word recognition, practically in favor of the interactive activation model. However, the limited number of event-related brain potential (ERP) studies have yielded inconsistent results considering this interaction's impact on N400 amplitude. The current ERP study aimed to examine whether the joint effects of stimulus quality and semantic priming were specific to the lexical decision task. We used both behavioral measures and ERP recordings to evaluate the joint effects of stimulus degradation (i.e. highly vs. slightly degraded) and semantic priming (i.e. semantically related vs. unrelated) in a lexical decision task involving visual recognition of Chinese characters. The results showed significant degradation-by-priming interactions on response times and N400 amplitude (P < 0.05), with larger semantic priming effects on slightly degraded targets. These converging behavioral and electrophysiological findings provide evidence in accordance with the interactive activation models of visual word recognition, in which the early-stage visual processing (i.e. degradation) cascades into the later-stage semantic processing (i.e. priming), thus yielding interactions observed in N400 amplitude.

A revised electrodiagnosis-based severity classification for carpal tunnel syndrome

BACKGROUND: An electrodiagnostic evaluation is conducted to diagnose carpal tunnel syndrome (CTS) and evaluate its severity. OBJECTIVE: This study proposes a revised approach for classifying the severity of electrophysiological findings for patients with CTS. METHODS: This retrospective cross-sectional study included patients with CTS confirmed through electrodiagnostic evaluations. Based on the Stevens’ classification, the patients were divided into three groups (mild/moderate/severe). A new intermediate group was defined to identify patients with normal motor nerve conduction studies and abnormal electromyographic results. CTS pain was evaluated using a numeric rate scale. Physical examinations and sonographic evaluation were performed to detect anatomical abnormalities. RESULTS: Overall, 1,069 CTS hands of 850 CTS patients were included. The mean age was 57.9 ± 10.8 years, and 336 (39.5%) were men. There were 522 (48.8%) mild cases; 281 (26.3%) moderate cases; and 266 (24.9%) severe cases. In the severe group, 49 cases were reclassified into the intermediate group. The median cross-sectional area in the intermediate group significantly differed from that in the severe group. However, the pain score significantly differed from that of the moderate group. CONCLUSION: The intermediate CTS group showed clinical features that were intermediate to those of the moderate and severe CTS groups.

The importance of medial plantar nerve conduction study in detectıon of polyneuropathy in inflammatory bowel disease

Background &amp; Objective: Peripheral neuropathy is the most frequent neurologic complication of inflammatory bowel disease (IBD). We aimed to evaluate the clinical utility of medial plantar nerve conduction study (NCS) in the detection of distal sensory polyneuropathy in IBD patients. Methods: The study was performed with 21 Crohn’s disease (Group 1) patients, 24 Ulcerative Colitis (Group 2) patients without clinical peripheral neuropathy and 28 healthy participants (Group 3). Each patient group underwent electrophysiological conduction studies. The findings were analyzed statistically. Results: Abnormal medial plantar nerve conduction was present on both sides in 11 (24.4 %) patients with IBD; 5 (11.1 %) patients had low sural nerve amplitude, and 5 (11.1 %) had low superficial peroneal nerve amplitude bilaterally. There were significant differences between the IBD groups (Group 1 and 2) and Group 3 in the mean sensory nerve action potential amplitude of the right medial plantar nerve (p&lt;0.024), and in the mean sensory nerve action potential amplitude of the left medial plantar nerve (p&lt;0.025). The polyneuropathy pattern was mostly of the sensory axonal type in patients with IBD. Conclusions: These electrophysiologic findings indicate that peripheral neuropathy is more prevalent in IBD. In IBD patients the amplitudes of the medial plantar nerve were abnormal more than in the sural and superficial peroneal nerves.

Clinical, etiological, and electrophysiological characteristics of patients with peripheral nerve damage caused by the February 6 earthquake in Türkiye

Objectives: This study aimed to analyze the clinical, etiological, and electrophysiological characteristics of the February 6 earthquake victims referred to our center due to nerve damage. Patients and methods: In this retrospective study, the demographic characteristics and findings of clinical examinations of 36 earthquake victims (25 females, 11 males; mean age: 31.6±15.5 years; range, 5 to 61 years) referred to our electrophysiology laboratory during the four-month period following the February 6 earthquake were investigated. The patients’ time spent under rubble, affected extremities, and electrophysiological findings were evaluated, and the locations of their lesions were determined using electromyography. Results: The mean time spent under rubble was 14.94±18.62 h, and 31 (86.1%) patients experienced partial nerve damage. Nerves were affected peripherally in 23 (74.2%) patients, at the lumbosacral plexus level in four (12.9%) patients, and at the brachial plexus level in another four (12.9%). Patients who were under rubble for more than 6.5 h had an increased risk of developing crush syndrome (p=0.014), and those under rubble for more than 8.5 h had an increased risk of developing compartment syndrome (p=0.008). Conclusion: The duration of exposure to rubble has been identified as a significant factor in the severity of nerve injury, as well as the development of compartment syndrome and crush syndrome. Therefore, the potential for peripheral nerve injury, which is a significant cause of morbidity, should be considered in the follow-up of patients who have survived earthquakes.

Correlation of Clinical and Electrophysiological Criteria in the Diagnosis of Guillain-Barré Syndrome: A Prospective Observational Study.

There are many criteria for diagnosing Guillain-Barré syndrome (GBS), and the yield of these diagnostic criteria varies. Each criterion requires some laboratory data and nerve conduction studies (NCS). Although supportive laboratory data are reassuring when present in suspected cases of GBS, when absent, they can potentially cause further delay in diagnosis and treatment. There is no gold standard test for the diagnosis of GBS, and there are multiple diagnostic criteria for GBS to date. The aim of the study is to know the sensitivity of different criteria, clinical and electrophysiological, for the diagnosis of GBS and to study the clinical spectrum and electrophysiological spectrum of GBS in our cohort of patients. We studied a total of 43 cases who presented with one or more of the following symptoms: relatively symmetrical and progressive flail-type weakness of more than one limb, with or without ataxia and/or ophthalmoplegia, and were diagnosed with GBS according to clinical criteria at the time of admission to Government Stanley Medical College Hospital. GBS mimics were ruled out. In all patients, the demographic data, cerebrospinal fluid (CSF) analysis (if done), and electrophysiological findings fitting into the diagnostic criteria of National Institute of Neurological Disorders and Stroke (NINDS), Dutch, and Brighton criteria were recorded. The need for assisted mechanical ventilation, neurology intensive care unit (NICU) stay, any complications, and treatment outcome details were recorded in a structured proforma. Most of the patients in our study were in their fourth decade of life, with a mean age of 41.37 years, similar to previous studies from India. Men are more frequently affected compared to women, similar to what has been observed in most studies done previously worldwide. In our study, electrophysiological criteria by Dutch criteria (87.5%), Brighton criteria (87.5%), and NINDS criteria (85.6%) had low sensitivity compared to the clinical criteria. In the present study, electrophysiological criteria proposed by the NINDS, Dutch, and Brighton criteria are less sensitive compared to clinical criteria in diagnosing GBS at early stages. Clinical criteria alone may be useful in resource-poor countries and at peripheral healthcare systems where NCS are not always readily available.

Switch to phagocytic microglia by CSFR1 inhibition drives amyloid-beta clearance from glutamatergic terminals rescuing LTP in acute hippocampal slices

Microglia, traditionally regarded as innate immune cells in the brain, drive neuroinflammation and synaptic dysfunctions in the early phases of Alzheimer disease (AD), acting upstream to Aβ accumulation. Colony stimulating factor 1-receptor (CSF-1R) is predominantly expressed on microglia and its levels are significantly increased in neurodegenerative diseases, possibly contributing to the chronic inflammatory microglial response. On the other hand, CSF-1R inhibitors confer neuroprotection in preclinical models of neurodegenerative diseases. Here, we determined the effects of the CSF-1R inhibitor PLX3397 on the Aβ-mediated synaptic alterations in ex vivo hippocampal slices. Electrophysiological findings show that PLX3397 rescues LTP impairment and neurotransmission changes induced by Aβ. In addition, using confocal imaging experiments, we demonstrate that PLX3397 stimulates a microglial transition toward a phagocytic phenotype, which in turn promotes the clearance of Aβ from glutamatergic terminals. We believe that the selective pruning of Aβ-loaded synaptic terminals might contribute to the restoration of LTP and excitatory transmission alterations observed upon acute PLX3397 treatment. This result is in accordance with the mechanism proposed for CSF1R inhibitors, that is to eliminate responsive microglia and replace it with newly generated, homeostatic microglia, capable of promoting brain repair. Overall, our findings identify a connection between the rapid microglia adjustments and the early synaptic alterations observed in AD, possibly highlighting a novel disease-modifying target.

Single simple question in axonal polyneuropathy.

The single simple question (SSQ), "What percentage of normal (0%-100%) do you feel regarding your disease?" has proven feasible and valid in assessing myasthenia gravis and a heterogeneous spectrum of neuropathies. This study explores the utility of the SSQ in axonal polyneuropathies (PNPs), encompassing diabetic neuropathy, and evaluates its responsiveness to scale changes. A retrospective chart review of 150 patients with axonal PNP responding to the SSQ was performed. Patients underwent clinical and electrophysiological evaluations, and were evaluated by clinical and disability scales, including the Medical Research Council sum score, modified Toronto Clinical Neuropathy score (mTCNS), Overall Neuropathy Limitation Scale, and Rasch-built Overall Disability Scale (RODS). The SSQ total scores correlated moderately with both the RODS score (r = .59, p < .001) and the mTCNS symptom score (r = -.43, p < .001), maintaining significance after adjustment for multiple comparisons. Longitudinally, after adjusting for multiple comparisons, the change in mTCNS symptom score retained statistical significance (adjusted p = .048). The SSQ did not show any association with electrophysiological parameters or sensory symptoms, other than a lower score in those with pain (100% with SSQ <40%, 85% with SSQ 40%-70%, and 34% with SSQ >70%). The SSQ is a feasible, valid scale that may be utilized to assess and follow patients with length-dependent axonal PNPs. Given that the SSQ is not strongly associated with clinical and disability scales or electrophysiological findings, additional investigations are required for a comprehensive assessment of PNP.

Sex-specific effects of subchronic NMDA receptor antagonist MK-801 treatment on hippocampal gamma oscillations.

N-methyl-D-aspartate (NMDA) receptor antagonists are widely used to pharmacologically model schizophrenia and have been recently established in the treatment of treatment-resistant major depression demonstrating that the pharmacology of this substance class is complex. Cortical gamma oscillations, a rhythmic neuronal activity associated with cognitive processes, are increased in schizophrenia and deteriorated in depressive disorders and are increasingly used as biomarker in these neuropsychiatric diseases. The opposite use of NMDA receptor antagonists in schizophrenia and depression raises the question how their effects are in accordance with the observed disease pathophysiology and if these effects show a consequent sex-specificity. In this study in rats, we investigated the effects of subchronic (14 days) intraperitoneal injections of the NMDA receptor antagonist MK-801 at a subanesthetic daily dose of 0.2 mg/kg on the behavioral phenotype of adult female and male rats and on pharmacologically induced gamma oscillations measured ex vivo from the hippocampus. We found that MK-801 treatment leads to impaired recognition memory in the novel object recognition test, increased stereotypic behavior and reduced grooming, predominantly in female rats. MK-801 also increased the peak power of hippocampal gamma oscillations induced by kainate or acetylcholine only in female rats, without affecting the peak frequency of the oscillations. The findings indicate that blockade of NMDA receptors enhances gamma oscillations predominantly in female rats and this effect is associated with behavioral changes in females. The results are in accordance with clinical electrophysiological findings and highlight the importance of hippocampal gamma oscillations as a biomarker in schizophrenia and depression.

High Neural Efficiency in Unconscious Perceptual Processing among Table Tennis Athletes: An Event-Related Potential Study.

Neural efficiency refers to the brain's ability to function with reduced resource expenditure while maintaining high performance levels. Previous research has demonstrated that table tennis athletes have greater neural efficiency at the conscious level. However, it is unknown whether they exhibit greater neural efficiency at the unconscious level. Therefore, this study aims to investigate unconscious perceptual processing and neural efficiency in elite table tennis athletes through tasks involving the judgment of spin serves. Fifty healthy, right-handed individuals participated in this study, including 25 elite table tennis athletes and 25 control participants without professional training experience. To evaluate the unconscious perceptual characteristics of both groups, we used a combination of masked priming paradigm and event-related potential techniques. The behavioral results reveal that, compared to the control group, the table tennis athletes displayed reduced reaction times (p < 0.001) and increased priming effects (p < 0.001) under unconscious conditions. The electrophysiological findings indicated that both groups elicited N1, N2, and P2 components. Notably, compared to the control group, the table tennis athletes exhibited significantly lower amplitude responses at the occipital lobe electrodes PO3, POz, PO4, O1, Oz, and O2 (p < 0.001). These results further support the neural efficiency hypothesis, indicating that prolonged professional training enhances athletes' capacities for specialized unconscious cognitive processing.

Risk factors and outcome of hyponatremia in patients with Guillain–Barré syndrome

The objective of the present study was to evaluate the risk factors and outcomes associated with hyponatremia in patients with Guillain-Barré syndrome (GBS). We retrospectively studied 80 consecutive patients with GBS who visited our hospital and compared clinical, laboratory, and electrophysiological findings of patients with and without hyponatremia. Disability was evaluated using the Hughes grading system. Of the 80 patients, 18 (23%) had hyponatremia. Hyponatremia was significantly associated with older age (P = 0.003), urinary retention (P < 0.0001), Hughes grade ≥ 4 at admission and nadir (P = 0.003 and P < 0.001, respectively), acute inflammatory demyelinating polyneuropathy subtype (P = 0.017), sepsis (P = 0.001), mechanical ventilator support (P = 0.013), longer hospitalization length of stay (P < 0.0001), and inability to walk independently at 6 months (P < 0.001). Multivariate analysis performed to assess the risk factors of hyponatremia revealed that urinary retention (odds ratio [OR] 30.7, 95% confidence interval [CI] 3.6–264.4; P = 0.002) and mechanical ventilator support (OR 13.8, 95% CI 1.6–118.0; P = 0.017) were significant independent risk factors of hyponatremia. In assessing the outcomes of patients with hyponatremia, multivariate analysis showed that hyponatremia was independently associated with hospitalization length of stay ≥ 60 days and inability to walk independently at 6 month, with the former showing statistical significance but the latter not (OR 9.3, 95% CI 1.8–47.7; P = 0.007 and OR 4.9, 95% CI 0.9–26.3; P = 0.066, respectively). Therefore, we demonstrate that, along with mechanical ventilator support, urinary retention—possibly indicating autonomic dysfunction—is a risk factor of hyponatremia in GBS. Moreover, we confirm that hyponatremia is associated with poor outcome in GBS.

A novel minimally invasive and versatile kyphoplasty balloon-based model of porcine spinal cord injury.

Spinal cord injury (SCI) animal models often utilize an open surgical laminectomy, which results in animal morbidity and also leads to changes in spinal canal diameter, spinal cord perfusion, cerebrospinal fluid flow dynamics, and spinal stability which may confound SCI research. Moreover, the use of open surgical laminectomy for injury creation lacks realism when considering human SCI scenarios. We developed a novel, image-guided, minimally invasive, large animal model of SCI which utilizes a kyphoplasty balloon inserted into the epidural space via an interlaminar approach without the need for open surgery. The model was validated in 5 Yucatán pigs with imaging, neurofunctional, histologic, and electrophysiologic findings consistent with a mild compression injury. Few large animal models exist that have the potential to reproduce the mechanisms of spinal cord injury (SCI) commonly seen in humans, which in turn limits the relevance and applicability of SCI translational research. SCI research relies heavily on animal models, which typically involve an open surgical, dorsal laminectomy which is inherently invasive and may have untoward consequences on animal morbidity and spinal physiology that limit translational impact. We developed a minimally invasive, large animal model of spinal cord injury which utilizes a kyphoplasty balloon inserted percutaneously into the spinal epidural space. Balloon inflation results in a targeted, compressive spinal cord injury with histological and electrophysiological features directly relevant to human spinal cord injury cases without the need for invasive surgery. Balloon inflation pressure, length of time that balloon remains inflated, and speed of inflation may be modified to achieve variations in injury severity and subtype.