northen diver
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Walter:
The Role of the Amygdala in Fear and Panic
Doug Holt
The definition of fear has proved to be an elusive mystery plaguing scientists. While there is much agreement as to the physiological effects of fear, the neural pathways and connections that bring upon these effects are not well understood. From the evolutionary standpoint, the theory is that fear is a neural circuit that has been designed to keep the organism alive in dangerous situations (1). How does it all work? Learning and responding to stimuli that warn of danger involves neural pathways that send information about the outside world to the amygdala, which in turn, determines the significance of the stimulus and triggers emotional responses like freezing or fleeing as well as changes in the inner workings of the body's organs and glands (1). There are important distinctions to make between emotions and feelings. Feelings are "red herrings", products of the conscious mind, labels given to unconscious emotions (2) whereas emotions are distinct patterns of behaviors of neurons. Emotions can exist of conscious experiencesas well as physiological and neurological reactions and voluntary and involuntary behaviors (3). But the components of fear goes beyond feelings and emotions. It is also the specific memory of the emotion. After a frightful experience, one can remember the logical reasons for the experience (e.g. the time and place) but one will also "feel" the memory, and his body will react as such (i.e. increased heart and respiration rate, sweating). In one recent case, after a near drowining incident, the victim could not only vividly remember each detail, but when doing so, his body reacted as though he were reliving the experience. These feelings of memory are stored in an almond shaped structure in the brain known as the amygdala.
. In the amygdala region alone, there is much controversy surrounding the nuclear subgroups, resulting in classifications that range between 5 and 22 different groups within the amygdala itself. Despite all of this, there are four main groups that have been universally agreed upon. These are the Basolateral, Lateral, Central, and Basomedial nuclei. The amygdala is considered to be the key component to the limbic system, a term that has also been regarded with much recent controversy by researchers in the field of emotions. When selectively electrically stimulated, the amygdala suppresses these behaviors and causes freezing. Freezing is a robust index of learned fear (16).
What is known about the amygdala is that it has a dual sensory input system. Both inputs run from the eyes, ears, and other sense organs to the thalamus. At that point the inputs diverge. One pathway leads directly to the amygdala while the other first passes through the cortex. Each input causes a distinct and specialized behavior. The amygdala is specialized for reacting to stimuli and triggering a physiological response, a process that would be described as the "emotion" of fear (2). After this, the stimuli of the activation of the amygdala is transmitted to the cortex. This is a distinct difference from a conscious feeling of fear. Feelings are thought arise from the second, slower pathway that travels from the sensory input first to the higher cortex and then to the amygdala. Its physiological effects are similar to the initial stages of fear. By having the body ready for action, the second circuit can then take a moment to analyze the signal in its entirety to determine whether or not the threat is real or perceived. If the threat is real, then the body is already on the go, if perceived, than nothing has been lost. But there are problems associated with the double wiring between the higher cortex and the amygdala. Unfortunately the neural connections from the cortex down to the amygdala are less well developed than are connections from the amygdala back up to the cortex. Thus, the amygdala exerts a greater influence on the cortex than vice versa. Once an emotion has been turned on, it is difficult for the cortex to turn it off (2).
Through the usage of fear conditioned rats in laboratory settings, researchers have been able to effectively map out the "fear circuit". The fear circuit is stimulated in rats by means of placing the animals in metal boxes and subjecting them to foot-shocks associated with an auditory signal. This method effectively conditions the rats to fear both the metal boxes in which they had experienced pain and the corresponding auditory signal. After experiencing these stimuli, the rats, when exposed to the auditory signal, react with fear. Occasionally, there can be debilitating problems associated with hyperactivity of the amygdala. Being the storehouse for the memory of fear, it can misinterpret signals from the body and cause inappropriate actions. This can lead to panic. Panic is a heightened stage of anxiety and fear feeding itself in a positive feedback loop and jumping to faulty conclusions, which focus on impending danger, madness, harm, or death. Physically, the body undergoes many changes that ready it for extreme action. There is a marked secretion of glucocorticoids and catecholamines which increases the blood glucose levels. Also, increase production of epinephrine and norepinephrine, which has the effect of vasodilation of blood vessels in skeletal muscles. Other symptoms of the sympatho-adrenergic stimulation involve modifications of breathing, increased temperature, localized sweating, decreased motility of the stomach, bowels, and intestines, constrictions of sphincters in the stomach and intestines, as well as piloerection (20). But the question of what generates panic attacks still remains essentially unanswered at the moment. There are many theories accorded to panic, the most prominent are:
Clark's theory on catastrophic interpretations (1988) sees panic attacks as a result of maladaptive and faulty interpretation of body signals. Beck's theory proposes a similar model, but based on predisposing and precipitating factors. Elhers' theory explains panic attacks as a result of panicogenic interoception. Barlow's theory proposes that panic attacks are modified "fight or flight" mechanisms in the absence of danger (20).
The limbic system, especially the amygdala, has long been considered to be directly implicated in anxiety and fear stages.
Fortunately, there are methods of reducing fear and inhibiting the fear response. Through testing with laboratory animals, it has been determined that when attention is shifted away from the anxiety-provoking stimulus, less fear is observed. When a novel stimulus is presented slightly before or at the same time as a well-trained condition stimulus, the condition response will be disrupted (18). This effect has been described using many methods but the neural mechanism is not well understood at this time. Another method of inhibiting the fear circuit is through conditioning. In a typical conditioned inhibition procedure, conditions are arranged such that one stimulus, denoted A, predicts shock, while another stimulus, denoted X, predicts absence of shock. The result of this procedure is that A comes to elicit a fear reaction when presented alone, but not when it is accompanied by X, the conditioned inhibitor (17). This is a similar method of treatment that is used for people with phobias. This method is inhibiting the emotional response produced by the amygdala during a threatening situation. The patient still remembers that he used to be afflicted by his phobia, but no longer has the emotional response attached to it (3). There is much correlation between the emotional states of fear. Anxiety, distress, and fear are closely related negative emotional states associated with physical or psychological harm. These three emotions can be differentiated by the temporal relationship between the feeling and the potential threat. Anxiety is characterized by the anticipation of being harmed in the future, where as fear is characterized as the anticipation of being harmed in the present. Distress is characterized by the awareness of being harmed at this particular moment. The three emotions can diffuse into one single diffuse state (5).
