The corticospinal tract, also known as the pyramidal tract, is the principal neural pathway mediating voluntary motor control. It connects the cerebral cortex to the spinal cord via the brainstem, enabling coordinated movement across skeletal muscles, as outlined in Figure 1. Originating in the frontoparietal cortices, corticospinal fibres converge into compact bundles as they descend through the brainstem, becoming increasingly condensed at the level of the pons [7]. Upon reaching the medulla, approximately 70–95% of fibres decussate at the pyramidal decussation, crossing to the contralateral side of the nervous system. The remaining fibres form the anterior corticospinal tract, which descends ipsilaterally and typically terminates at the lower thoracic levels of the spinal cord, located in the mid-back region. Within the spinal cord, fibres travel through the anterior and lateral corticospinal tracts before synapsing onto anterior horn neurons of the grey matter. These neurons project to axial and limbal muscles, ultimately enabling voluntary motor function [7]. 

The basal ganglia are a group of subcortical nuclei situated deep within the forebrain that play a central role in the regulation of motor control. Beyond movement, they contribute to reasoning, adaptive behaviour, reward-based learning, motivation, and cognitive processes involved in initiating and completing actions. Their close relationship with the cerebral cortex allows them to be organised into discrete, functionally specialised cortico-basal ganglia loops [8]. Rather than providing diffuse cortical access to the motor system, these circuits support parallel processing across motor and non-motor domains. Consequently, damage to basal ganglia circuits linked to motor cortical regions primarily produces motor deficits, whereas disruption of non-motor circuits results in higher-order cognitive and behavioural impairments [8].

The interaction between emotional and motor systems is therefore mediated by specialised neural circuits that integrate sensory, cognitive, and affective information to guide behaviour [1]. A key node in this interface is the nucleus accumbens, a structure within the basal ganglia that is well positioned to translate emotional states into action. The nucleus accumbens receives convergent input from emotion-related regions, including the amygdala, and projects to non-motor related structures, enabling emotional signals to influence locomotor and orofacial motor responses [1].

Fear as a survival motor programme

Fear is widely regarded as a primary emotion, with its neural underpinnings classically linked to the amygdala. It is defined as an aversive emotional state arising from the anticipation or perception of actual or potential danger. One of the most extensively studied models of emotional learning is classical Pavlovian fear conditioning, particularly in animal research [9]. In this paradigm, a neutral stimulus, commonly a tone, is repeatedly paired with an aversive unconditioned stimulus, such as a mild electric shock. Following conditioning, the previously neutral stimulus alone elicits species-specific fear responses, including freezing or escape behaviours, autonomic changes such as increased heart rate and blood pressure, and neuroendocrine responses such as stress hormone release. Through this process, newly learned threats gain access to evolutionarily conserved neural programmes that support adaptive responses to danger [9].

Extensive evidence demonstrates that lesions of the amygdala disrupt both the acquisition and expression of conditioned fear. Within the amygdala, the basolateral complex serves as a critical site of sensory convergence and stimulus association, integrating cortical and subcortical inputs during fear learning [9]. In contrast, the central nucleus projects to downstream regions involved in executing fear responses, including the hypothalamus, and is widely considered a primary output pathway for conditioned fear. Lesions to either region disrupt both learning and expression of fear responses, supporting this functional organisation [9]. 

Fear-related behaviours are further mediated by projections within the prefrontal cortex–amygdala–periaqueductal grey pathway, which exerts top-down modulation over the descending inhibitory pain system. The prefrontal cortex processes nociceptive and aversive information and maintains reciprocal connections with the amygdala, while the periaqueductal grey integrates emotional, cognitive, and behavioural responses to threat [10]. Studies of fear-conditioned analgesia, which is the reduction in pain sensitivity upon re-exposure to a conditioned aversive stimulus, have provided key insights into endogenous pain suppression and its relationship with fear [10]. The dorsal periaqueductal grey plays a central role in this process, mediating both conditioned and unconditioned fear responses through activation of descending inhibitory pathways. The basolateral and central nuclei of the amygdala provide major output to the dorsal periaqueductal grey, linking emotional processing with pain modulation. Electrophysiological evidence further indicates that potentiation of the amygdala–periaqueductal grey pathway is associated with anxiety-like behaviours in animal models [10].

The phrase “fight or flight” is commonly used to describe behavioural responses to threat, yet it is often misinterpreted as reflecting conscious emotional choice. In reality, these responses represent the activation of distinct, evolutionarily conserved motor programmes. Humans possess a repertoire of innate defensive behaviours, collectively termed the defence cascade, that are automatically recruited in response to threat [11]. Fight and flight represent active defensive strategies, freezing reflects a temporary suspension of action, and tonic immobility emerges as a last-resort response to inescapable danger. Each state is characterised by a distinct neural signature involving coordinated activity across the amygdala, hypothalamus, periaqueductal grey, and autonomic nuclei [11].

While many animals rapidly return to baseline functioning once danger has passed, humans often remain locked into recurrent defensive patterns long after the original threat or trauma has resolved. Understanding the neural components that generate these responses is therefore critical for developing effective therapeutic interventions [11]. Such approaches aim to selectively modulate elements of defensive circuitry, shifting the associated neural pattern and corresponding mind-body state. Central to this framework is the recognition that subjective fear emerges after the body has already been biased toward action, constraining the range of available behaviours before conscious emotional awareness fully develops [11].

Stress-induced biasing of action control and decision-making

Stress is a pervasive feature of everyday life and can be conceptualised as a state of sustained action readiness without resolution. Like fear, stress engages evolutionarily conserved defensive systems that bias the body toward action before conscious deliberation occurs. Stressful situations vary in intensity, producing a spectrum of emotional and behavioural responses closely aligned with the defence cascade [12]. Individuals are frequently required to make decisions under stress, particularly when perceived threat is high or when time and cognitive resources are limited. Under these conditions, decision-making strategies often shift, resulting in choices that differ markedly from those made in low-stress contexts. These effects are best understood through the lens of motor biasing rather than impaired reasoning alone [12].

From an evolutionary perspective, the stress response enhances survival in situations requiring rapid action. Physiological adaptations, including increased heart rate, deeper respiration, elevated glucose availability, thermoregulatory sweating, and heightened muscle tension, prepare the body for movement and prioritise speed over deliberation [12]. At the cognitive level, stress biases behaviour toward intuitive, low-effort strategies. Under normal conditions, intuitive impulses are evaluated by prefrontal control systems that allow for flexible planning and inhibition. Under stress, however, top-down control is weakened, allowing default and habitual motor programmes to be released with minimal modification [12].

Neurobiologically, stress impairs prefrontal cortex functions such as working memory, attention regulation, and response inhibition, while increasing reliance on bottom-up signalling from subcortical regions including the amygdala and basal ganglia. Neuroimaging studies show that acute stress reduces connectivity between ventromedial and dorsolateral prefrontal cortex regions involved in self-control, limiting goal-directed action selection and favouring habitual responses [12].

Critically, the behavioural effects of stress are best characterised as a narrowing of available actions rather than a loss of rationality. Stress constrains behavioural freedom by biasing the motor system toward a restricted set of survival-relevant responses before conscious awareness emerges. Although this may be subjectively experienced as feeling ‘trapped’, it reflects a body that has already committed to defensive pathways in advance of conscious choice [12].

Neural effects of positive emotions on behavioural flexibility

Research has historically prioritised threat-related emotions and their effects on behaviour, yet emotion-action coupling cannot be fully understood without considering positive emotional states. In contrast to fear and stress, which narrow behavioural options, positive emotions broaden the momentary thought–action repertoire, supporting the accumulation of enduring personal resources across physical, cognitive, social, and psychological domains [13].

Positive emotions bias the motor system toward approach and continued engagement rather than defensive withdrawal. Theoretical frameworks consistently suggest that positive affect promotes exploration, persistence, and interaction with the environment. Whereas neutral states may leave individuals disengaged, positive emotions increase the likelihood of approaching novel objects, people, or situations, supporting adaptive development at both individual and species levels [13].

Positive emotional states generate internal signals that promote initiation or continuation of action, although these signals are less rigidly specified than those associated with threat. Sensory pleasure motivates approach toward biologically relevant stimuli, while diffuse positive moods encourage persistence in ongoing activities [13]. Discrete emotion theories link joy with aimless activation, interest with attentional engagement, and contentment with behavioural quiescence. Although these tendencies are less specific, they nonetheless reflect consistent links between emotional state and motor expression, as seen in energetic or animated behaviours associated with excitement and joy [13].

Positive emotions typically arise in non-life-threatening contexts, where rapid behavioural narrowing is unnecessary. Rather than suppressing alternative actions, positive affect expands behavioural possibilities, increasing flexibility and choice. Emotions such as joy, interest, contentment, excitement, pride, and love thus widen the set of available actions, directly counteracting the constraining effects of fear and stress [13].

While threat-related emotions confer immediate adaptive benefits, the broadened repertoires associated with positive emotions yield indirect and long-term advantages. Through exploration and engagement, positive emotional states build durable personal resources that persist beyond the transient emotional experience. These resources form reserves that can later be drawn upon when individuals encounter stress or threat, enhancing resilience and adaptive capacity over time [13].

Conclusion

Across emotional states ranging from fear and stress to joy and excitement, a unifying principle emerges: emotions do not simply follow action, but actively shape the body’s readiness to act. Rather than functioning as conscious directives, emotions bias motor systems by preparing, constraining, or releasing specific patterns of behaviour through coordinated neural circuits involving the prefrontal cortex, basal ganglia, amygdala, periaqueductal grey, and corticospinal pathways. Threat-related emotions engage evolutionarily conserved defence programmes that narrow behavioural options to prioritise survival, whereas positive emotions expand the action repertoire, fostering exploration, learning, and resilience. Stress represents a prolonged state of action readiness in which inhibitory control is weakened and behavioural freedom becomes constrained before conscious awareness emerges. Together, these findings challenge the traditional view of emotion as a purely subjective experience that precedes action. Instead, emotion emerges as a dynamic biological mechanism that sculpts the action landscape itself, determining not only what a person feels, but what they are able to do.