Spontaneous Facial Expressions and Micro-expressions Coding: From Brain to Face

Facial expressions are a vital way for humans to show their perceived emotions. It is convenient for detecting and recognizing expressions or micro-expressions by annotating a lot of data in deep learning. However, the study of video-based expressions or micro-expressions requires that coders have professional knowledge and be familiar with action unit (AU) coding, leading to considerable difficulties. This paper aims to alleviate this situation. We deconstruct facial muscle movements from the motor cortex and systematically sort out the relationship among facial muscles, AU, and emotion to make more people understand coding from the basic principles: We derived the relationship between AU and emotion based on a data-driven analysis of 5,000 images from the RAF-AU database, along with the experience of professional coders.We discussed the complex facial motor cortical network system that generates facial movement properties, detailing the facial nucleus and the motor system associated with facial expressions.The supporting physiological theory for AU labeling of emotions is obtained by adding facial muscle movements patterns.We present the detailed process of emotion labeling and the detection and recognition of AU.Based on the above research, the video's coding of spontaneous expressions and micro-expressions is concluded and prospected.

The course of facial corticobulbar tract fibers in the dorsolateral medulla oblongata

Background The course of the corticobulbar tract (CBT) to the facial nucleus has been investigated by some previous studies. However, there are some unclear points of the course of the CBT to the facial nucleus. This study aimed to elucidate the detailed course of the CBT to the facial nucleus through the analysis of lateral medullary infarction (LMI) cases. Methods The neurological characteristics and magnetic resonance imaging findings of 33 consecutive patients with LMI were evaluated. The location of the lesions was classified rostro-caudally (upper, middle, or lower) and horizontally. Further, we compared the neurological characteristics between the groups with and without central facial paresis (FP). Results Eight (24%) patients with central FP ipsilateral to the lesion were identified. Dysphagia and hiccups were more frequently observed in the group with central FP than in the group without central FP. In patients with central FP, middle medullary lesions and those including the ventral part of the dorsolateral medulla were more frequently observed. Contrastingly, patients with lesions restricted to the lateral and dorsal regions of the dorsolateral medulla did not present with central FP. Conclusion The results of this study indicate that the CBT to the facial nucleus descends with the corticospinal tract at least to the middle portion of the medulla, and then ascends to the facial nucleus through the medial and ventral areas of the dorsolateral medulla after decussation.

Prosaposin and its receptors GRP37 and GPR37L1 show increased immunoreactivity in the facial nucleus following facial nerve transection

Neurotrophic factor prosaposin (PS) is a precursor for saposins A, B, C, and D, which are activators for specific sphingolipid hydrolases in lysosomes. Both saposins and PS are widely contained in various tissues. The brain, skeletal muscle, and heart cells predominantly contain unprocessed PS rather than saposins. PS and PS-derived peptides stimulate neuritogenesis and increase choline acetyltransferase activity in neuroblastoma cells and prevent programmed cell death in neurons. We previously detected increases in PS immunoactivity and its mRNA in the rat facial nucleus following facial nerve transection. PS mRNA expression increased not only in facial motoneurons, but also in microglia during facial nerve regeneration. In the present study, we examined the changes in immunoreactivity of the PS receptors GPR37 and GPR37L1 in the rat facial nucleus following facial nerve transection. Following facial nerve transection, many small Iba1- and glial fibrillary acidic protein (GFAP)-positive cells with strong GPR37L1 immunoreactivity, including microglia and astrocytes, were observed predominately on the operated side. These results indicate that GPR37 mainly works in neurons, whereas GPR37L1 is predominant in microglia or astrocytes, and suggest that increased PS in damaged neurons stimulates microglia or astrocytes via PS receptor GPR37L1 to produce neurotrophic factors for neuronal recovery.

Deletion of CD38 and supplementation of NAD+ attenuate axon degeneration in a mouse facial nerve axotomy model

Following facial nerve axotomy, nerve function is not fully restored even after reconstruction. This may be attributed to axon degeneration/neuronal death and sustained neuroinflammation. CD38 is an enzyme that catalyses the hydrolysis of nicotinamide adenine dinucleotide (NAD+) and is a candidate molecule for regulating neurodegeneration and neuroinflammation. In this study, we analyzed the effect of CD38 deletion and NAD+ supplementation on neuronal death and glial activation in the facial nucleus in the brain stem, and on axon degeneration and immune cell infiltration in the distal portion of the facial nerve after axotomy in mice. Compared with wild-type mice, CD38 knockout (KO) mice showed reduced microglial activation in the facial nucleus, whereas the levels of neuronal death were not significantly different. In contrast, the axon degeneration and demyelination were delayed, and macrophage accumulation was reduced in the facial nerve of CD38 KO mice after axotomy. Supplementation of NAD+ with nicotinamide riboside slowed the axon degeneration and demyelination, although it did not alter the level of macrophage infiltration after axotomy. These results suggest that CD38 deletion and supplementation of NAD+ may protect transected axon cell-autonomously after facial nerve axotomy.

Respiratory Central Pattern Generator: Microcircuit Generation of the Rhythms and Patterns of Breathing

Breathing is a vital rhythmic motor behavior that mediates gas exchange to support metabolism and regulate pH. All mammals must breathe continuously and reliably from birth and modulate their breathing throughout life in response to changes in metabolic demand and environmental stimuli. A number of congenital and neurodegenerative disorders affect the neural control of breathing in humans and lead to serious adverse health consequences, even death. Since the previous edition of this book, there have been considerable advances in our understanding of the breathing central pattern generator (CPG). This chapter focuses on the neural microcircuit within the preBötzinger Complex (preBötC); a second oscillator near the facial nucleus that appears to generate active expiration; and the microcircuit for sighing.