Comparison of resting electroencephalogram coherence in patients with mild cognitive impairment and normal elderly subjects

Mild cognitive impairment (MCI) was a condition beginning before more serious deterioration, leading to Alzheimer’s dementia (AD). MCI detection was needed to determine the patient's therapeutic management. Analysis of electroencephalogram (EEG) coherence is one of the modalities for MCI detection. Therefore, this study investigated the inter and intra-hemispheric coherence over 16 EEG channels in the frequency range of 1-30 Hz. The simulation results showed that most of the electrode pair coherence in MCI patients have decreased compared to normal elderly subjects. In inter hemisphere coherence, significant differences (p<0.05) were found in the FP1-FP2 electrode pairs. Meanwhile, significant differences (p<0.05) were found in almost all pre-frontal area connectivity of the intra-hemisphere coherence pairs. The electrode pairs were FP2-F4, FP2-T4, FP1-F3, FP1-F7, FP1-C3, FP1-T3, FP1-P3, FP1-T5, FP1-O1, F3-O1, and T3-T5. The decreased coherence in MCI patients showed the disconnection of cortical connections as a result of the death of the neurons. Furthermore, the coherence value can be used as a multimodal feature in normal elderly subjects and MCI. It is hoped that current studies may be considered for early detection of Alzheimer’s in a larger population.

Prefrontal connectomics: from anatomy to human imaging

The fundamental importance of prefrontal cortical connectivity to information processing and, therefore, disorders of cognition, emotion, and behavior has been recognized for decades. Anatomic tracing studies in animals have formed the basis for delineating the direct monosynaptic connectivity, from cells of origin, through axon trajectories, to synaptic terminals. Advances in neuroimaging combined with network science have taken the lead in developing complex wiring diagrams or connectomes of the human brain. A key question is how well these magnetic resonance imaging (MRI)-derived networks and hubs reflect the anatomic “hard wiring” first proposed to underlie the distribution of information for large-scale network interactions. In this review, we address this challenge by focusing on what is known about monosynaptic prefrontal cortical connections in non-human primates and how this compares to MRI-derived measurements of network organization in humans. First, we outline the anatomic cortical connections and pathways for each prefrontal cortex (PFC) region. We then review the available MRI-based techniques for indirectly measuring structural and functional connectivity, and introduce graph theoretical methods for analysis of hubs, modules, and topologically integrative features of the connectome. Finally, we bring these two approaches together, using specific examples, to demonstrate how monosynaptic connections, demonstrated by tract-tracing studies, can directly inform understanding of the composition of PFC nodes and hubs, and the edges or pathways that connect PFC to cortical and subcortical areas.

Movement-Dependent Electrical Stimulation for Volitional Strengthening of Cortical Connections in Behaving Monkeys

Correlated activity of neurons can lead to long-term strengthening or weakening of the connections between them. In addition, the behavioral context, imparted by execution of physical movements or the presence of a reward, can modulate the plasticity induced by Hebbian mechanisms. In the present study, we have combined behavior and induced neuronal correlations to strengthen connections in the motor cortex of adult behaving monkeys. Correlated activity was induced using an electrical-conditioning protocol in which stimuli gated by voluntary movements were used to produce co-activation of neurons at motor-cortical sites involved in those movements. Delivery of movement-dependent stimulation resulted in small increases in the strength of associated cortical connections immediately after conditioning. Remarkably, when paired with further repetition of the movements that gated the conditioning stimuli, there were substantially larger gains in the strength of cortical connections, that occurred in a use-dependent manner, without delivery of additional conditioning stimulation. In the absence of such movements, little change was observed in the strength of motor-cortical connections. Performance of the motor behavior in the absence of conditioning also did not produce any changes in connectivity. Our results show that combining movement-gated stimulation with further natural use of the “conditioned” pathways after stimulation ends can produce use-dependent strengthening of connections in adult primates, highlighting an important role for behavior in cortical plasticity. Our data also provide strong support for combining movement-gated stimulation with use-dependent physical rehabilitation for strengthening connections weakened by a stroke or spinal-cord injury.Significance StatementWe describe an electrical-conditioning protocol in adult behaving monkeys in which stimuli gated by voluntary movements were used to strengthen connections between motor-cortical neurons involved in those movements. Movement-gated stimulation created a plastic landscape in which repetition of the movements that gated conditioning stimuli produced strengthening of cortical connections, in a use-dependent manner, long after stimulation had ended, a finding that is both novel and unique. In the absence of such behavior, little change was observed in the strength of connections. Similarly, movements alone did not produce any changes in connectivity. Our data highlight a critical role for behavior in plasticity and provide strong support for combining movement-gated stimulation with use-dependent rehabilitation for strengthening connections weakened by injury or disease.

Muscle Tone Physiology and Abnormalities

The simple definition of tone as the resistance to passive stretch is physiologically a complex interlaced network encompassing neural circuits in the brain, spinal cord, and muscle spindle. Disorders of muscle tone can arise from dysfunction in these pathways and manifest as hypertonia or hypotonia. The loss of supraspinal control mechanisms gives rise to hypertonia, resulting in spasticity or rigidity. On the other hand, dystonia and paratonia also manifest as abnormalities of muscle tone, but arise more due to the network dysfunction between the basal ganglia and the thalamo-cerebello-cortical connections. In this review, we have discussed the normal homeostatic mechanisms maintaining tone and the pathophysiology of spasticity and rigidity with its anatomical correlates. Thereafter, we have also highlighted the phenomenon of network dysfunction, cortical disinhibition, and neuroplastic alterations giving rise to dystonia and paratonia.

A critical period of neuronal activity results in aberrant neurogenesis rewiring hippocampal circuitry in a mouse model of epilepsy

In the mammalian hippocampus, adult-born granule cells (abGCs) contribute to the function of the dentate gyrus (DG). Disruption of the DG circuitry causes spontaneous recurrent seizures (SRS), which can lead to epilepsy. Although abGCs contribute to local inhibitory feedback circuitry, whether they are involved in epileptogenesis remains elusive. Here, we identify a critical window of activity associated with the aberrant maturation of abGCs characterized by abnormal dendrite morphology, ectopic migration, and SRS. Importantly, in a mouse model of temporal lobe epilepsy, silencing aberrant abGCs during this critical period reduces abnormal dendrite morphology, cell migration, and SRS. Using mono-synaptic tracers, we show silencing aberrant abGCs decreases recurrent CA3 back-projections and restores proper cortical connections to the hippocampus. Furthermore, we show that GABA-mediated amplification of intracellular calcium regulates the early critical period of activity. Our results demonstrate that aberrant neurogenesis rewires hippocampal circuitry aggravating epilepsy in mice.

The Experience of Using the Original Complex of Physiotherapy Exercises and Electrical Stimulation during Rehabilitation of the Patient with Pseudobulbar Paralysis

Pseudobulbar paralysis is neurological pathology caused by the interruption of cortical connections with the motor nuclei of the medulla oblongata of various etiologies. Aim: to describe the original complex of kinesitherapy for pseudobulbar syndrome, adequate to the competencies of physiotherapy exercises instructors and available for home use by relatives of patients. Material and methods. The object of observation was a patient with post-traumatic pseudobulbar syndrome, manifested by dysphagia, hypersalivation, anarthria, and bilateral central prosopoplegia. The methods of endo-oral and acupressure massage were used as well as the blockade of trigger points along the interested muscle-tendon meridians. Therapeutic gymnastics techniques were used based on friendly reaction, initiating the activity of the paretic lingual and laryngeal-pharyngeal muscles with the help of their unaffected agonists which were supplemented by electrical stimulation with impulse currents. Results. The observed two-year catamnesis indicates the presence of a positive effect when using this approach. Conclusion. The described methods of pseudobulbar paralysis kinesitherapy are simple and intuitive, they are suitable for development by nurses, social workers and relatives of patients, which allows them to be used at the third stage of rehabilitation.