Academic literature on the topic 'Impulse circuits'

Aggression can be categorized into three subtypes: premeditated aggression, frustration-related aggression, and impulsive aggression (IA), which is the focus of this chapter. It first delineates the social information processing model of IA and its neurobiological underpinnings, with a special focus on ventral prefrontal-amygdala, frontostriatal, and frontoparietal circuits. In these circuits, structural as well as functional alterations have been associated with IA. A large body of basic and clinical research has examined the role of neurotransmitters (glutamate, GABA) and neuromodulators (monoamines and neuropeptides) in mediating IA. The important role of the monoamines dopamine, serotonin, norepinephrine, and acetylcholine in the mediation of different aspects of IA and the pharmacological potential resulting from these alterations are depicted in the second half of the chapter. The chapter concludes with an overview of the most important etiological factors.

Impulse control disorders (ICDs) are common disabling disorders that have impulsive behavior as a core feature. They emerge early in life and run a chronic lifelong course. They are assumed to lie at the severest end of a continuum of impulsivity that connects normal with pathological states. People with ICDs experience a drive to undertake repetitive acts. Although the consequences are damaging, performance of the impulsive act may be experienced as rewarding, or alternatively may relieve distress, implicating dysfunction of the neural circuitry involved in reward processing and/or behavioral inhibition. Clinical data are increasingly pointing toward an etiological association between some ICDs, such as pathological gambling and addiction, and others, such as trichotillomania and compulsive disorders. Comorbidity with other psychiatric disorders is also common, and hints at overlapping psychobiological processes across several diagnostic groups. The results of neurocognitive studies suggest that impulsivity is multidimensional and comprises dissociable cognitive and behavioral indices governed by separate underlying neural mechanisms. For example, trichotillomania may primarily involve motor impulsivity, whereas problem gambling may involve reward impulsivity and reflection impulsivity. Exploring neurocognitive changes in individuals with ICDs and other mental disorders characterized by poor impulse control, and among their family members, may help to elucidate the underpinning neurocircuitry and clarify their nosological status.

Aggression is a behavior with evolutionary origins, but in today’s society it’s often both destructive and maladaptive. The fact that aggression has a strong basis in biological factors has long been apparent from case histories of traumatic brain damage. Research over the past several decades has confirmed the involvement of neurotransmitter function and abnormalities in brain structure and function in aggressive behavior. This research has centered around the “serotonin hypothesis” and on dysfunction in prefrontal brain regions. As this literature continues to grow, guided by preclinical research and aided by the application of increasingly sophisticated neuroimaging methodology, a more complex picture has emerged, implicating diverse neurotransmitter and neuropeptide systems (e.g., glutamate, vasopressin, and oxytocin) and neural circuits. As the current pharmacological and therapeutic interventions are effective but imperfect, it is hoped that new insights into the neurobiology of aggression will reveal novel avenues for treatment of this destructive and costly behavior.

Atrial flutter is the term given to one of the four types of supraventricular tachycardia; in it, atrial activation occurs as a consequence of a continuous ‘short circuit’: a defined and fixed anatomical route, resulting in a fairly uniform atrial rate, and uniform atrial flutter waves on the ECG. The ventricles are not a part of this arrhythmia circuit, and ventricular activation is variable, dependent on atrioventricular (AV) nodal conduction. Given that the atrial rate is essentially uniform (e.g. 300 min−1), ventricular activation tends to be regular (i.e. 150 min−1, 100 min−1, 75 min−1, etc., if the atrial rate is 300 mins−1), or regularly irregular if changes are occurring in the fraction of conducted impulses to the ventricles. When AV nodal conduction permits only 4:1 conduction or less, atrial flutter is usually obvious, but when ventricular rates are higher (150 min−1 or more) the flutter waves can be obscured by the QRS complexes, making diagnosis more difficult. Atrial flutter is of two types, typical and atypical. Typical atrial flutter is a right atrial tachycardia, with electrical activation proceeding around the tricuspid valve annulus. This arrhythmia is dependent on a zone of slow electrical conduction through the cavotricuspid isthmus (the tissue lying between the origin of the inferior vena cava and the posterior tricuspid valve). The resulting circuit can be either anticlockwise (activation proceeds up the inter-atrial septum, across the atrial roof, down the free wall, and then through the cavotricuspid isthmus to the basal septum) or clockwise (down the inter-atrial septum and around the circuit in the opposite direction). Anticlockwise typical atrial flutter is more common. Atypical atrial flutter refers to all other atrial flutters, and this includes other right atrial flutters (e.g. pericristal flutter), left atrial flutters, post-ablation or post-surgical flutters, and pulmonary vein flutters. The feature common to all types of flutter and which differentiates flutter from other types of supraventricular tachycardia is the presence of a macro-re-entrant anatomical circuit around which the electrical impulse travels continuously and repeatedly, thereby generating the flutter. Even though typical atrial flutter has a fairly obvious and specific appearance on the ECG, atypical flutters do not, and often it is only possible to differentiate atypical flutter from atrial tachycardias by invasive electrophysiology studies, as the ECG alone may be insufficient.

Chapter 7 takes the investigation of the aesthetic impulse into the human brain to understand, first, why only we—and not our closest relatives among the primates—express ourselves aesthetically; and second, how the brain reacts when presented with aesthetic material. Brain scans are less useful when you are interested in the Why of aesthetic behavior rather than the How. Nevertheless, some brain studies have been ground-breaking, and neuroaesthetics offers a pivotal argument for the key function of the aesthetic impulse in human lives; it shows us that the brain’s reward circuit is activated when we are presented with aesthetic objects and stimuli. For why reward a perception or an activity that is evolutionarily useless and worthless in relation to human existence?