Neural control and its contributing to social behavior

Anonymous
timer Asked: Dec 9th, 2018

Question description

I just did a paper with someone else and it was awfully bad and it has a polgarism.So, I need someone to help me to edit it or if it possible to redo it again and make it perfect as the requirements asked. The paper basically is talking about a control system that influence in human movement .The system that I choice is orbitofrontal cortex.Can someone write how is this system influence in human movement. ( like this system is responsible for face expression) choice any input that orbitofrontal cortex control it . and also include and explore in details the feature of the system like what is the input , output , modulating component and the feedback. and also the annotated diagram has to be shown . I will attach an example of paper that the prof asked us to do it similarly. and I have attached a diagram that the prof help me and clarify for me how would be the paper about my topic.

Neural control and its contributing to social behavior
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Running head: SOCIAL BEHAVIOR AND NEURAL CONTROL Social Behavior and Neural Control Student Name Institutional Affiliation 0 0 SOCIAL BEHAVIOR AND NEURAL CONTROL 1 Social Behavior and Neural Control Introduction Generally, human social behavior is subject to neural control. One of the main control systems influencing social behavior is the orbitofrontal cortex. The orbitofrontal cortex is significantly related to human emotions and decision making process. It located right above the eye sockets and it is directly connected to the sensorial areas, as well as the structures of the limbic system that are related to emotion and memory. Basically, human social skills require the ability to adapt and regulate instinctive reactions to emotional signals. Such important emotional signals include the communicative signals of threat or appeasement that are often conveyed by emotional facial expressions in humans. It is important to realize that this particular ability is not at all trivial, as demonstrated by the inability of non-human primates to control their approach and avoidance tendencies, particularly when engaged in activities involving collaborations. It is worth realizing that several studies have addressed the neural bases of perception of social emotional signals, particularly facial expressions. Studies have highlighted the role of the amygdale, along with other limbic structures in the process of automatically processing of facial expressions (Beer et al., 2006). There are important cerebral and cognitive mechanisms that control the behaviors that are often evoked by such perceptual processes. Many studies have recognized the role of orbitofrontal cortex in the voluntary regulation of human emotions, as well as in the control of social emotional behavior. More specifically, the lateral orbitofrontal cortex, along with the adjacent ventrolateral prefrontal cortex is primarily involved in the selection of actions that serve to override automatic and motivationally driven response tendencies. It is also believed that the role of orbitofrontal cortex extends to the domain of social approach avoidance behavior. As such, orbitofrontal cortex influences the social emotional behavior. It is worth SOCIAL BEHAVIOR AND NEURAL CONTROL 2 noting that several studies have operationalized social approach avoidance behavior by asking individuals to move their forearm either towards their body or away from their body in response to emotional face stimuli. Essentially, when individual subjects approach angry faces and avoid happy faces, their reaction times are slower compared to when they approach happy faces and avoid angry faces. Approaching angry faces and avoiding happy faces is considered an incongruent condition while approaching happy faces and avoiding angry faces is considered a congruent condition. It is important to realize that response time effect is an indication that during incongruent trials, the individual subjects have to solve the task by overriding their instinctive response tendencies. Basically, humans are normally conditioned to avoid angry faces and approach happy faces. However, when the conditions are reversed, subjects have to put efforts to override the automatic responses. The approach avoid congruency effect is particularly linked to the generation of an explicit emotional judgment. Additionally, responses mappings are often used in tasks that need the evaluation of an affectively irrelevant attribute of the same stimuli, such as the gender of a face. Therefore, orbitofrontal cortex plays a significant role in the processing of social emotions, thus influencing individual social behavior. Impact of Orbitofrontal Cortex on Social Behavior The orbitofrontal cortex influences the processing of social emotions in humans as it is linked to the limbic system and the amygdale. This indicates that the orbitofrontal cortex articulates the emotions related to social behavior such as aggressiveness, interacting with others adequately, and lack of respect. It is also important to realize that the orbitofrontal cortex has the a surveillance system that is responsible for making individuals effectively adapt and behave according to the context they find themselves in, making them control their basic impulses. SOCIAL BEHAVIOR AND NEURAL CONTROL 3 The orbitofrontal cortex also influences human behavior as a response to the rewards or punishments received. For instance, researchers have established that patients whose orbitofrontal cortexes are damaged are more likely to stop being sensitive to punishments. This may significantly hinder a balanced and harmonious coexistence in a social environment. The OFC is also linked to the human decision making process (Beer et al., 2006). Several studies have established that human motivation, particularly when wanting to take the initiative to do something is located in the orbitofrontal cortex. People without a well functioning orbitofrontal cortex may not be able to tell which option is the safest and most prudent. Neurophysiology of the Orbitofrontal Cortex Taste Essentially, the orbitofrontal cortex contains a major representation of taste. It is worth noting that taste can play the role of a primary enforcer. The stimulus-reinforcement association learning lay a fundamental understanding of the role of the orbitofrontal cortex. Basically, the representation of taste in the orbitofrontal cortex encompasses robust representations of the prototypical tastes of salt, sweet, sour, and bitter. It is important to realize that the nature of the representation of taste in the OFC is that the reward value of the taste is represented (De Araujo et al., 2003). The evidence for this phenomenon is that the responses of the orbitofrontal taste neurons are modulated by hunger. Research has shown that the orbitofrontal cortex taste neurons stop responding to the taste of food with which it is fed on to satiety. In human neuro-imaging experiments, it has been established that there is an orbitofrontal cortex area that is activated by sweet taste, and that there are partly separate areas that are activated by the aversive taste of saline. The ventral frontal region of the orbitofrontal cortex has been implicated in the olfactory processing in humans. Research has shown that the representation of the olfactory stimulus was SOCIAL BEHAVIOR AND NEURAL CONTROL 4 independent of its association with taste reward. Additionally, the odors to which a particular neuron responded is influenced by test with which the odor is associated. In order to effectively analyze the nature of the olfactory representation in the orbitofrontal cortex, the responses of the olfactory neurons that responded to food while the monkeys were fed to satiety were measured. It was established that the majority of the orbitofrontal olfactory neurons decreased their responses to the odor of the food with which the monkey was fed to satiety. Thus, for the neurons, the reward value of the odor is basically what is actually represented in the orbitofrontal cortex. Visual Inputs in the Orbitofrontal Cortex Generally, there is significant visual input in many neurons in the orbitofrontal cortex. Additionally, what is normally represented by the neurons is often the reinforcement association of the visual stimuli. The visual input is usually from the ventral, temporal lobe, the visual stream, concerned with what object is actually being seen (Carmichael & Price, 1994). Thus, the orbitofrontal cortex visual neurons always respond differentially to objects or images based on their reward association. Essentially, the primary reinforce that has been utilized is taste. Many of the orbitofrontal cortex show visual-taste reversal in one or a very few trials. Therefore, the conditional reward neurons serve to convey information regarding the current reinforcement status of a certain stimuli, and may reflect the fact that not all the neurons which learn associations to primary reinforcers are able to sample the complete space of all the possible conditioned stimuli, particularly when acting as a pattern. Another important type of information that is represented in the orbitofrontal cortex is the information about faces. It is important to note that there is a population of orbitofrontal neurons which respond in many ways like those in the temporal cortical visual areas. The SOCIAL BEHAVIOR AND NEURAL CONTROL 5 orbitofrontal face-responsive neurons were first observed in 1983 by Thorpe and others. The orbitofrontal face-responsive neurons tend to respond with longer latencies compared to temporal lobe neurons. The orbitofrontal face responsive neurons normally convey information regarding which face is being seen. Because these neurons have different responses to different faces, they are typically harder to activate strongly compared to temporal cortical face-selective neurons, as many of them respond much better to real faces than two-dimensional images of faces on a video monitor. Most importantly, the orbitofrontal cortex face-selective neurons are responsive to face movement or gesture. Such findings are consistent with the likelihood that such neurons are activated through inputs from the temporal cortical visual areas in which the face selective neurons are located (Butter et al., 1970). This is because the faces convey important information that is critical for social reinforcement in at least two ways implemented by the neurons. Firstly, some of the neurons may encode facial expression, which can serve to indicate reinforcement. Secondly, the neurons encode information regarding which individual is present, which based on stimulus-reinforcement association learning is important in the evaluation and utilization of learned reinforcing inputs, and particularly in social situations. The social situation could be the current reinforcement value as decoded by the stimulus reinforcement association of a certain individual. Research has show that activation of a part of the human orbitofrontal cortex takes place during a face discrimination reversal task. In the task, the faces of two different people are displayed, and when the correct face is selected, the expression turns into a smile. After a certain period of correct performance, the contingencies are reversed, and the other face has to be selected to obtain a smile expression as a reinforcer. The research established that activation of a SOCIAL BEHAVIOR AND NEURAL CONTROL 6 part of the orbitofrontal cortex occurred particularly in relation to the reversal. This implies that there is a part of the orbitofrontal cortex that responds selectively in relation to face expression particularly when it indicates that behavior should change in humans. Neuroimaging In order to elucidate the role of the human orbitofrontal cortex in emotion, researchers carried out an investigation aimed at determining where the pleasant affective component of touch is represented in the brain. Basically, touch is one of the important reinforcers that can produce pleasure. The researchers established using fMRI that a weak but very pleasant touch of the hand with velvet resulted in a much stronger activation of the orbitofrontal cortex compared to a more intense but affectively neutral touch of the hand with wood. The research established that the affective neutral but more intense touch produced more activation of the primary somatosensory cortex than the pleasant stimuli. The findings demonstrate that a part of the orbitofrontal cortex is responsible for the representation of the positively affective aspects of the somatosensory stimuli. One of the most significant findings of the study is that the primary reinforcer that can produce affectively positive emotional responses is essentially represented in the human orbitofrontal cortex. The finding forms a fundamental basis for the human orbitofrontal cortex to be involved in the stimulus-reinforcement association learning that lays the foundation for emotional learning in humans. Studies have also shown that there is also a representation of the affective negative aspects of touch such as pain in the human orbitofrontal cortex. The finding confirms reports that humans with damage on the ventral part of the frontal lobe may report that they know that a stimulus is pain producing, but the pain does not feel very bad to them. Stimulus-Reinforcement Association and Reversal SOCIAL BEHAVIOR AND NEURAL CONTROL 7 The reversal of learning that takes place in the orbitofrontal cortex could actually be implemented by Hebbian modification of the synapses responsible for conveying visual input onto taste responsive neurons. This results in the implementation of a pattern association network. It is important to realize that long term potentiation could play a significant role in strengthening the synapses from active conditional stimulus neurons onto neurons that respond to such primary reinforcers as sweet taste. On the other hand, homo-synaptic long-term depression could significantly weaken synapses from the same active visual inputs, particularly if the neurons were not responding due to an aversive primary reinforcer such as the taste of saline. It is important to note that the conditional reward neurons in the human orbitofrontal cortex relay information regarding the current reinforcement status of a given stimuli, and may also reflect the fact not every neuron which learns association to primary reinforcers such as taste can actually sample the complete space of all the possible conditioned stimuli, especially when acting as a pattern associator. However, such neurons can play an important role in conveying very useful information, as they indicate that one of the stimuli to which they are capable of responding is currently associated with reward. It is also important to point out that such neurons also serve to punish primary reinforcers (Deco & Rolls, 2003). Research has also shown that very rapid, one trial, reversal that is a property of visual orbitofrontal cortex neurons may actually require a short term memory attractor network necessary for retaining the current rule. Additionally, a small degree of synaptic adaptation in such a rule network would effectively provide for the alternative rule state to emerge after the attractor is quenched by a non-reward signal. SOCIAL BEHAVIOR AND NEURAL CONTROL 8 Additionally, the error-detector neurons, which are responsible for responding, particularly during frustrative non-reward could be a result of a mismatch between what was expected when the stimulus was shown and the primary reinforcer that was obtained. Prefrontal Cortex Neural Networks Essentially, the orbitofrontal cortex remembers the most recent reward association of stimuli through its stimulus-reinforcer association learning, and implements it by synaptic plasticity (Deco & Rolls, 2004). This implies that that no ongoing neuronal firing is required to implement stimulus-reinforcer association memory. On the contrary, the inferior convexity prefrontal cortex and the dorsolateral prefrontal cortex usually implement a short term memory for stimuli that is often maintained by the active continuing firing of neurons. Continuous firing of neurons during a short term memory period after the end of a stimulus is a common way used by the brain to effectively implement short term memory. Consequences of Broken or Diseased Orbitofrontal Cortex Broken or diseased orbitofrontal cortex has significant adverse effects on an individual’s social behavior. Damage in human orbitofrontal cortex may later behavior, especially when stimulus-reinforcement associations are modified (Szczepanski & Knight, 2014). As such, humans with orbitofrontal cortex damage can exhibit impairments in a number of tasks, particularly those in which an alteration of behavioral strategy is required in response to a change in environmental reinforcement contingencies. Additionally, individuals with injured orbitofrontal cortex could actually stop being sensitive to punishments, indicating that changing their behaviors for the better could be hard. Such people may not care about the consequences of their actions (Zhan et al., 2014). However such people could have an obsession with rewards. If they fail to get their rewards they are more SOCIAL BEHAVIOR AND NEURAL CONTROL 9 likely to become impulsive, frustrated, and aggressive. Damage to the orbitofrontal cortex could impair an individual’s decision making capacity. It is common for such people to make a decision that makes them to go back to the original problem. It is also important to note that people with damaged orbitofrontal cortex usually have psychological challenges. They may become rude, develop problems in social interactions, abuse drugs, become hypersexual, and exhibit criminal behavior. New Research on Orbitofrontal Cortex Latest research has focused on the role of orbitofrontal cortex in guiding behavior. Scientists recognize the decision making largely depends on the ability to infer the consequences of our potential behavior (Baltz et al., 2018). As such, the orbital frontal cortex has been hypothesized to underlie such a predictive capability, with orbitofrontal cortex representing hidden state task space that functions to combine predictive information with memories of perceptually similar rewards or sensory information to control future behavior. In line with such an hypothesis, orbitofrontal cortex appears necessary to infer outcome representations from predictive cues that follow a reduction in the desirability of that outcome (Baltz et al., 2018). In order to effectively examine state dependent control over decision making, the researchers examined how changes in state alter action control independent of changes in action contingency. Additionally, the researchers established that orbitofrontal cortex activity is necessary for incentive learning processes in general following a state change. SOCIAL BEHAVIOR AND NEURAL CONTROL 10 References Beer, J. S., John, O. P., Scabini, D., & Knight, R. T. (2006). Orbitofrontal cortex and social behavior: integrating self-monitoring and emotion-cognition interactions. Journal of cognitive neuroscience, 18(6), 871-879. Beyer, F., Münte, T. F., Göttlich, M., & Krämer, U. M. (2014). Orbitofrontal cortex reactivity to angry facial expression in a social interaction correlates with aggressive behavior. Cerebral cortex, 25(9), 3057-3063. Butter, C. M., Snyder, D. R., & McDonald, J. A. (1970). Effects of orbitofrontal lesions on aversive and aggressive behaviors in rhesus monkeys. Journal of Comparative and Physiological Psychology, 72, 132–144. Carmichael, S. T., & Price, J. L. (1994). Architectonic subdivision of the orbital and medial prefrontal cortex in the macaque monkey. Journal of Comparative Neurology, 346, 366– 402. Carmichael, S. T., Clugnet, M.-C., & Price, J. L. (1994). Central olfactory connections in the macaque monkey. Journal of Comparative Neurology, 346, 403–434. De Araujo, I. E. T., Kringelbach, M. L., Rolls, E. T., & McGlone, F. (2003b). Human cortical responses to water in the mouth, and the effects of thirst. Journal of Neurophysiology, 90, 1865–1876. SOCIAL BEHAVIOR AND NEURAL CONTROL 11 De Araujo, I. E. T., Rolls, E. T., Kringelbach, M. L., McGlone, F., & Phillips, N. (2003c). Tasteolfactory convergence, and the representation of the pleasantness of flavour, in the human brain. European Journal of Neuroscience, 18, 2059–2068. Deco, G., & Rolls, E. T. (2003). Attention and working memory: a dynamical model of neuronal activity in the prefrontal cortex. European Journal of Neuroscience, 18, 2374–2390. Gunaydin, L. A., Grosenick, L., Finkelstein, J. C., Kauvar, I. V., Fenno, L. E., Adhikari, A., ... & Tye, K. M. (2014). Natural neural projection dynamics underlying social behavior. Cell, 157(7), 1535-1551. Szczepanski, S. M., & Knight, R. T. (2014). Insights into human behavior from lesions to the prefrontal cortex. Neuron, 83(5), 1002-1018. Zhan, Y., Paolicelli, R. C., Sforazzini, F., Weinhard, L., Bolasco, G., Pagani, F., ... & Gross, C. T. (2014). Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior. Nature neuroscience, 17(3), 400.
BE 421/521 Final Paper / Presentation Final Paper Rough draft: Due Thursday, November 29th, 2018 in class so that you can exchange the rough draft with a classmate and give each other constructive feedback. Final draft: Due Thursday, Dec 13th, 2018 during exam session The final paper is a written report of a particular control system involved in human movement. The paper should introduce your system of choice, describe the impact of this system on human movement, and explore in detail the features of the system (inputs, outputs, modulating components, feedback, etc.). You may wish to consider what occurs when this system is broken/diseased, and new avenues of research involving this system. Use structured subheadings to improve the clarity and organization of your paper. Be sure to include your annotated diagram and refer to it in the text! Your paper should: • • • • • • • Be 9 pages (undergraduate) or 12 pages (graduate) excluding references Use 12-point font Be double-spaced Have 1” margins Include your annotated diagram (and other diagrams as necessary) Have clear writing without typos … please enlist a friend or family member to proofread your work! Include at least 10 primary source articles. The references should be cited in the text like this (Johnson et al., 2014) with the full references in a section after your text like this: References (the first ref below is for journal articles, the second is for a book) Johnson UA, Movement NC, Control F (2014) How to include references in your paper topic. Journal of our class 1(2): 203-204. Zancolli E (1979) Structural and dynamic bases of hand surgery. Philadelphia: Lippincott. Final Presentations • This is an oral presentation of your final paper. • Presentations will be on December 6th and 13th. We will decide on the order of presenters after the Thanksgiving break. • Presentations will be 10 – 12 minutes in length, followed by a few minutes for questions from me and the rest of the class. You are expected to ask questions to other presenters at some point and will be given participation points based on this. • Plan on preparing 8 – 12 slides for your presentation. 1 – 2 minutes per slide is a good rule of thumb for presentations.
Babinski Reflex 1.0 Introduction The Babinski reflex is a common assessment tool used by neurologists for determining the integrity of spinal reflexes and the corticospinal tract. It is stimulated by stroking the sole of the foot with a blunt instrument (Mortimer, Maricle, Neuhaus, & Konstam, 2011) (Fig. 1). Specifically, the reflex is elicited by running the object along the lateral plantar border of the foot near the heel, crossing the metatarsal pads (i.e. ball of the foot) and ending near the hallux (i.e. big toe) (Khwaja; Van Gijn, 1995) (Fig. 1). If this stroking motion causes hallux dorsiflexion, also known as hallux extension, the response is considered normal in infants. Paradoxically, the hallux extensors (in anatomical terms) are considered flexor muscles in a physiological sense. Thus, hallux dorsiflexion and extension describe the same movement, the movement of the hallux closer to the shin, while hallux plantar flexion and flexion describe the opposite movement (Van Gijn, 1995). Hallux dorsiflexion during the Babinski reflex test is considered abnormal if it persists after the age of two (Kumar, 2003; Pauc; Walker, Hall, & Hurst, 1990). Figure 1. A typical commercially available Babinski hammer (left) (http://mdpocket.com/telescopicbabinski-reflex-hammer.html). The metal side of the object should be pressed against the skin. The blunt ends of reflex hammers and thumbnails are also commonly used. Path that the object should follow (right). The naming convention for resulting hallux dorsiflexion or plantar flexion is called a positive and negative Babinski sign, respectively. This terminology is named after the French neurologist, Joseph Babinski, who first discovered this phenomenon at the end of the 19th century (Bruno, Horacio, Yolanda, & Guillermo). The purpose of this paper is to provide an indepth review of the control mechanisms involved in the Babinski reflex and how the maturing brain can modulate reflexes. It will also describe how a positive Babinski sign in non-infants can be used to help diagnose a lesion in the central nervous system. The Babinski reflex in infants is first described in detail, followed by the reflex in adults. 2.0 Infants 2.1 Phalangeal Dorsiflexion Foot stimulation from the blunt object is detected by cutaneous receptors in the S1 dermatome, an area of skin that is mainly supplied by a single spinal nerve. The afferent signal then travels up the tibial and sciatic nerves to the L5/S1 nerve root to the dorsal horn of the spinal cord (Fig. 2). It then travels via interneurons, neurons that serve as the connection point between sensory and motor pathways, in the spinal cord to the anterior horn to elicit a motor response (Futagi & Suzuki, 2010). Given that this reflex does not involve higher level control above the spinal cord in infants, it is a spinal reflex (Futagi, Suzuki, Toribe, & Kato). A motor response in this spinal reflex occurs via an efferent command from the L5/S1 nerve roots to first the sciatic nerve and then the tibial and deep peroneal nerves. The deep peroneal nerve then innervates the extensor hallucis longus muscle (Fig. 3). This muscle arises from the middle portion of the fibula on the anterior surface of the interosseous membrane and inserts on the dorsal side of the base of the distal phalanx of the hallux. Since the muscle runs along the top of the foot and inserts on the top of the hallux, when activated it causes dorsiflexion of the hallux (Fig. 4). The extensor digitorum longus is also commonly activated during the Babinski reflex. Since this muscle originates on the anterior lateral condyle of the tibia and inserts on the dorsal surface of the middle and distal phalanges of the lateral four digits, it dorsiflexes and abducts or 2 fans outs the other phalanges of the foot (Deng, Jia, Zhang, Guo, & Yang). Since the hallux has the largest degree of movement of all the phalanges due to the anatomical structure of the metatarso-phalangeal joints, movement of the hallux is usually the greatest and therefore the easiest to monitor during the reflex (Dafkin et al.). Figure 2. Neural control behavior during a positive Babinski sign. Figure 3. The positive Babinski reflex involves the activation of the extensor hallucis longus which dorsiflexes the hallux and frequently also activates the extensor digitorum longus which dorsiflexes the other phalanges. 3 Figure 4. A 5-month old involuntary eliciting a positive Babinski sign (red circle) by accidently applying pressure along the sole of his left foot with the hallux of his right foot. Figure annotated from (Neelon, 1999). 2.2 Involvement of Leg Flexors as Part of Flexion Withdrawal Reflex The muscles involved in a positive Babinski sign are responsible for shortening the leg, consistent with a more general flexion withdrawal reflex that protects the body from painful stimuli by shortening the limb and removing the limb from the stimuli (Dafkin et al.; Deng et al.; Sandrini, Serrao, Rossi, & Romaniello). For example, during a positive Babinski sign, the contraction of the extensors of the phalanges occurs in combination with activation of the tibialis anterior, the hamstrings (i.e. semitendinosus, semimembranosus and biceps femoris) and the tensor fasciae latae muscle (Van Gijn, 1995) (Fig. 5). The tibialis anterior originates on the lateral (outside) surface of the tibia and inserts into the medial cuneiform and first metatarsal of the foot and acts to dorsiflex and invert the foot (turn the bottom of the foot inward). The hamstrings originate on the tuberosity of the ischium and linea aspera (ridge of roughened surface on the posterior surface of the femur), and insert on the tibia and fibula. They act to flex the knee and extend the hip. The tensor fasciae latae originates on the iliac crest and inserts on the iliotibial tract and acts to flex the thigh, along with also medially rotating and abducting the thigh. In summary, these muscles primarily act to flex and thus shorten the leg (Hultborn). 4 However, since the big toe is lighter than the foot, shank, and thigh, the activation of these muscles during the Babinski reflex rarely causes noticeable movement of these body segments. As will be explained in detail below, as the central nervous system matures, the dorsiflexion of the phalanges are no longer part of the flexion withdrawal reflex, while the foot, thigh and leg flexors all remain part of the flexion withdrawal reflex. Figure 5. The tibialis anterior, hamstring and tensor fasciae latae are also activated during a positive Babinski sign as part of the flexion withdrawal reflex, although usually not at a sufficient magnitude to cause visible movement of the foot, shank or thigh. 3.0 Adults 3.1 Negative Babinski Sign 3.1.1 Phalangeal Decoupling from Flexion Withdrawal Reflex The corticospinal tract is a group of about 1 million nerves that originate in layer V of the cerebral cortex, primarily from the primary motor cortex (30%) (M1), supplementary motor area (SMA) and the premotor cortex (30%), and the somatosensory cortex (S1), parietal lobe and cingulate gyrus (40%) (Walker et al., 1990). The nerves travel from the cortex down to the spinal cord and cross over at the ventral surface of the medulla in the brainstem (Fig. 6). Individual nerves terminate at the vertebral level of the muscle that they innervate. However, most of the nerves do not directly synapse with nerves of the peripheral nervous system such as 5 the sciatic nerve, but instead synapse with interneurons. At birth, the corticospinal tract is unmyelinated, but progressively myelinates during the first two years of life (Deng et al.). Figure 6. Neural control during a negative Babinski sign. The corticospinal tract is fully myelinated by around age two, enabling them to inhibit hallux dorsiflexion via the interneurons. After age two, the Babinski reflex normally results in a negative sign, suggesting the myelination of the corticospinal tract is the driving factor in the change in the direction of hallux movement occurring around that age (Deng et al.). Myelination of the corticospinal tract enables the tract to inhibit the interneurons that cause the hallux to dorsiflex. Thus, corticospinal involvement in the control of movement represents a higher level of involvement in the central nervous system (CNS), meaning above the spine or supraspinal. This supraspinal involvement decouples the phalanges from the more general flexion withdrawal reflex, causing the Babinski reflex to become a cutaneous reflex (Nakajima, Sakamoto, Tazoe, Endoh, & Komiyama). 6 3.1.2 Cutaneous Reflex Cutaneous reflexes are activated by skin receptors and play a valuable role in locomotion. They are important in responses to obstacles or stumbling and for making adjustments to unexpected stimuli (Nakajima et al.). A common result of a cutaneous reflex is the activation of extension muscles that act to propel the limb and body away from the stimuli (Van Gijn, 1995). A negative Babinski sign is caused by activation of the flexor hallucis longus muscle. This muscle originates on the fibula and inserts on the plantar surface of the foot at the base of the distal phalanx of the hallux (Fig. 7). Since it runs along the bottom of the foot, its activation causes the hallux to plantar flex. This motion is similar to toe-off during walking or running and acts to propel the body forward. Commonly, the flexor digitorum longus muscle is also activated. This muscle originates on the posterior surface of the tibia and inserts on the plantar surface of the foot, on the base of the distal region of the 2nd through 5th phalanges and therefore acts to plantar flex those phalanges (Fig. 7). Again, the activation of these phalangeal flexor muscles during the Babinski reflex requires a healthy and mature central nervous system that enables the corticospinal tract to inhibit the flexion withdrawal of the hallux (Chew, Oon, Lee, Lim, & Tan; Khwaja). Interestingly, for a sleeping healthy adult, the reflex will revert back to being positive, providing proof that inhibition of the response involves brain activation in an awake state, even if it is subconscious (Singerman & Lee). 7 Figure 7. A negative Babinski reflex involves the activation of the flexor hallucis longus (left) which plantar flexes the hallux and frequently also activates the flexor digitorum longus (right) which plantar flexes the other phalanges. 3.2 Positive Babinski Sign in Adults 3.2.1 Testing of Phalangeal and Leg Flexors A positive Babinski sign in non-infants is a sign of damage to the corticospinal tract such that it can no longer inhibit interneurons at the sacral level of the spine and the central nervous system reverts to its neonatal, or primitive, setting (Neelon, 1999). The control mechanisms that result in hallux dorsiflexion in adults are the same that cause hallux dorsiflexion to occur in infants (Fig. 2). However, many factors need to be considered prior to concluding that the reflex results in a positive sign in adults. For example, the change in hallux angle is not objectively quantified and is only observed by the clinician. Moreover, the threshold that should be considered abnormal is not well defined (Mortimer et al.). For example, some clinicians might consider hallux dorsiflexion of less than 15° worrisome, while others might consider it to be inconclusive or inconsequential. Therefore, movement of the hallux should not be the only variable considered during the test (Van Gijn, 1995). As stated above, during a positive Babinski sign, other limb flexors, such as the tibialis anterior, the hamstrings and the tensor fasciae latae muscle are activated during a positive Babinski sign since it is part of a more general flexion withdrawal reflex. The examiner can either palpate over these muscles during the test to feel if 8 they tighten or try to observe the thigh, shank and foot for movement to confirm a positive Babinski sign (Van Gijn, 1995). The examiner should also palpate the extensor hallucis longus muscle during the test to confirm that it tightens. This can help rule out hallux dorsiflexion occurring from passive movement. Additionally, the reflex should be conducted on both feet, and the tests should not be considered abnormal unless the change in hallux angle in dorsiflexion is clearly asymmetrical, compared to the ipsilateral side (Mortimer et al.). 3.2.2 Other Stimulation Tests and Reliability of Babinski Reflex Other stimulation tests that produce Babinski-like responses are usually also conducted to confirm a positive Babinski sign. These include stroking the lateral malleolus (Chaddock sign), applying pressure down the medial side of the tibia (Oppenheim sign), squeezing the calf (Gordon sign) or Achilles tendon (Schaeffer sign), or flexing and then quickly releasing the fourth phalanx (Gonda sign) (Mortimer et al.). However, the Babinski sign is considered the most reliable of these tests since it has the highest reported inter-rater consistency, with a kappa value (i.e. the degree of agreement actually achieved above chance divided by the degree of agreement that is attainable above chance) of 0.5491 (Singerman & Lee). By comparison, the Chaddock, Oppenheim, and Gordon reflexes have kappa values of 0.4065, 0.3739, and 0.3515, respectively (Singerman & Lee). Besides the previously described qualitative instead of quantitative assessment of the change in hallux angle, one the other biggest factors of inter-rater and intra-rater inconsistencies in these tests is that they are conducted manually by the examiner, introducing a high degree of variability in the duration of stroke and maximum and average force applied during the tests (Dafkin et al.; Ross, Velez-Borras, & Rosman). This likely influences the interpretation of these tests since the Spearman’s rank correlation between duration of stroke, maximum and average force and change in hallux angle all have significance values (p) of equal 9 to or less than 0.01 (Dafkin et al.). Moreover, there is a wide range of sensitivity (i.e. actual positives which are correctly identified, also known as the true positive rate) and specificity (i.e. the proportion of negatives which are correctly identified, also known as the true negative rate) values reported for the Babinski reflex. The published sensitivity and specificity values range from 20 – 80% and 80 – 96%, respectively (Cook, Hegedus, Pietrobon, & Goode; Miller & Johnston). As a whole, the lower sensitivity values and higher specificity values appear to make it more likely that someone with a corticospinal tract lesion will have a negative Babinski sign, compared to a healthy individual having a positive Babinski sign. Given the above uncertainties with the Babinski reflex, it should not be the only test conducted during a neurological exam and other tests should be conducted to validate its findings (Cook et al.). 3.2.3 Cortical vs. Sub-cortical Lesions While a positive Babinski sign cannot be used to determine the exact location of the lesion to the corticospinal tract, there has been research on whether isolated hallux dorsiflexion compared to hallux dorsiflexion in combination with dorsiflexion and fanning out of the 2nd through 5th phalanges can be used to determine whether the lesion is cortical or subcortical (Deng et al.). Specifically, 107 subjects with lesions of the corticospinal tract confirmed with medical imaging were put into two groups: 1) Sub-cortical lesions, with lesion in the corona radiata to spinal cord (n = 93); and 2) Cortical lesions (n = 14) (Fig. 8). Of the 93 patients in the sub-cortical group, 4% had isolated hallux dorsiflexion and 96% had recruitment of the other phalanges. By contrast, in the cortical group, 71% had isolated hallux dorsiflexion and 29% had dorsiflexion and/or fanning out of other phalanges. The authors concluded that since the corticospinal fibers are more centralized within the brainstem and vertebral canal, a small lesion in the spinal cord can bring about more generalized symptoms due to a greater number of 10 neurons affected, whereas a lesion in the cortex likely affects less pathway fibers because the fibers are more diffuse in the cortex (Deng et al.). In essence, the fibers are bundled together in the smaller volume of the spinal cord and thus a lesion at that location causes more generalized symptoms since it affects more fibers at that bottle-neck location. Figure 8. Example of lesions, identified by arrows, from cortical (left) and sub-cortical groups (right). The cortical lesion group mostly had isolated hallux dorsiflexion, while the sub-cortical group had combined hallux and 2nd through 5th phalangeal dorsiflexion and fanning out. 3.2.4 Follow-up Clinical Testing and Imaging Although the degree of phalangeal involvement may help determine if the lesion is cortical or sub-cortical, a positive Babinski sign cannot be used to make a differential diagnosis since a positive sign can be caused by a wide range of diseases related to compromised spinal cord and brain function. These include a lesion impinging the spinal cord, a brain tumor along the corticospinal tract, meningitis, multiple sclerosis, stroke, rabies, amyotrophic lateral sclerosis (ALS), hepatic encephalopathy, and cerebral palsy (Mortimer et al.). A combination of followup brain and spine MRIs, cerebral angiography, lumbar puncture, cerebrospinal fluid (CSF) analysis, and somatosensory evoked potentials (SEP) are usually needed to make a differential diagnosis about the classification and exact location of the lesion to the corticospinal tract 11 (Mortimer et al.). Individuals who have a positive Babinski sign usually have concomitant weakness, incoordination and general difficulty with muscle control, alerting the physician to a potential problem prior to testing the Babinski reflex. However, the testing of the Babinski reflex is a quick, easy and cheap clinical test for neurologist to use to determine if the pathology involves the corticospinal tract prior to ordering expensive and time consuming clinical testing and imaging. 4.0 Conclusion The purpose of this paper was to provide an in-depth review of the control mechanisms involved in the Babinski reflex and how the maturing brain can modulate reflexes. In infants, the Babinski reflex results in hallux dorsiflexion since it is part of the more general flexion withdrawal reflex. This is a spinal reflex with no higher input above the spinal cord. During the first two years of life, the corticospinal tract myelinates and inhibits hallux dorsiflexion during the Babinski reflex and from being part of the flexion withdrawal reflex. The decoupling of hallux dorsiflexion from the flexion withdrawal reflex causes the Babinski reflex to become a cutaneous reflex, which involves higher input from the brain. Thus, in healthy adults, the Babinski reflex results in hallux plantar flexion. A reversal of hallux movement from plantar flexion to dorsiflexion (positive Babinski sign) in adults is a sign of damage to the corticospinal tract. A positive Babinski finding in adults can be caused by a myriad of diseases and conditions that affect the corticospinal tract. Although movement of the 2nd and 5th phalanges during the Babinski reflex can help determine whether damage to the tract is cortical or sub-cortical, further testing is required to determine the exact location and cause of the damage to the tract. Nonetheless, the Babinski reflex remains a valuable and inexpensive test for determining the integrity of spinal reflexes and the corticospinal tract. 12 References Bruno, E., Horacio, S.-M., Yolanda, E., & Guillermo, G. R. (2007). The articles of Babinski on his sign and the paper of 1898. Neurology India, 55(4), 328. Chew, K., Oon, L., Lee, R., Lim, K., & Tan, C. (2010). Withdrawal response in healthy adults. Neurology Asia, 15(2), 159-165. Cook, C. E., Hegedus, E., Pietrobon, R., & Goode, A. (2007). A pragmatic neurological screen for patients with suspected cord compressive myelopathy. Physical therapy, 87(9), 12331242. Dafkin, C., Green, A., Kerr, S., Raymond, A., Veliotes, D., Elvin, A., . . . McKinon, W. (2014). Kinematic and kinetic analysis of the inter-and intra-applicator assessment of the Babinski reflex. Neurophysiologie Clinique/Clinical Neurophysiology, 44(5), 471-477. Deng, T., Jia, J.-p., Zhang, T., Guo, D., & Yang, L. (2013). Cortical versus non-cortical lesions affect expression of Babinski sign. Neurological Sciences, 34(6), 855-859. Futagi, Y., & Suzuki, Y. (2010). Neural Mechanism and Clinical Significance of the Plantar Grasp Reflex in Infants. Pediatric neurology, 43(2), 81-86. Futagi, Y., Suzuki, Y., Toribe, Y., & Kato, T. (1999). Neurologic outcomes of infants with tremor within the first year of life. Pediatric neurology, 21(2), 557-561. Hultborn, H. (2006). Spinal reflexes, mechanisms and concepts: from Eccles to Lundberg and beyond. Progress in neurobiology, 78(3), 215-232. Khwaja, G. A. (2005). Plantar reflex. Journal Indian Academy of Clinical Medicine, 6(3), 193197. Kumar, S. P. (2003). The Babinski sign--a critical review. Journal of the Association of Physicians of India, 51, 53-57. Miller, T. M., & Johnston, S. C. (2005). Should the Babinski sign be part of the routine neurologic examination? Neurology, 65(8), 1165-1168. Mortimer, J. E., Maricle, D. E., Neuhaus, D., & Konstam, E. (2011). Babinski Reflex Encyclopedia of Child Behavior and Development (pp. 197-199): Springer. Nakajima, T., Sakamoto, M., Tazoe, T., Endoh, T., & Komiyama, T. (2006). Location specificity of plantar cutaneous reflexes involving lower limb muscles in humans. Exp Brain Res, 175(3), 514-525. Neelon, F. A. (1999). Babinski Sign. Corsini Encyclopedia of Psychology. Pauc, R. (2011). The Babinski sign in sickness and in health. Clinical Chiropractic, 14(3), 122126. Ross, E. D., Velez-Borras, J., & Rosman, N. P. (1976). The Significance of the Babinski Sign in the Newborn—A Reappraisal. Pediatrics, 57(1), 13-15. Sandrini, G., Serrao, M., Rossi, P., & Romaniello, A. (2005). The lower limb flexion reflex in humans. Progress in neurobiology, 77(6), 353-395. Singerman, J., & Lee, L. (2008). Consistency of the Babinski reflex and its variants. European Journal of Neurology, 15(9), 960-964. Van Gijn, J. (1995). The Babinski reflex. Postgraduate medical journal, 71(841), 645-648. Walker, H. K., Hall, W. D., & Hurst, J. W. (1990). Clinical methods. 13

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