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==Anxiety== | ==Anxiety== | ||
'''Anxiety''' is an elevated physiological state marked by demonstrable changes in [[Cognition|cognitive]], [[Somatic|somatic]], [[Emotion|emotional]], and [[Behavior|behavioral]] components <ref>Seligman, M.E.P., Walker, E.F. & Rosenhan, D.L. (2001). ''Abnormal psychology'', (4th ed.) New York: W.W. Norton & Company, Inc.</ref> These components combine to create the feelings that we typically recognize as [[fear]], [[apprehension (fear)|apprehension]], or [[worry]]. Anxiety is often accompanied by physical sensations such as | '''Anxiety''' is an elevated physiological state marked by demonstrable changes in [[Cognition|cognitive]], [[Somatic|somatic]], [[Emotion|emotional]], and [[Behavior|behavioral]] components <ref>Seligman, M.E.P., Walker, E.F. & Rosenhan, D.L. (2001). ''Abnormal psychology'', (4th ed.) New York: W.W. Norton & Company, Inc.</ref> These components combine to create the feelings that we typically recognize as [[fear]], [[apprehension (fear)|apprehension]], or [[worry]]. Anxiety is often accompanied by physical sensations such as [[heart palpitations]], [[nausea]], [[chest pain]], [[shortness of breath]], [[stomach aches]], or [[tension headache|headache]]. The cognitive component entails expectation of a diffuse and certain danger. Somatically the body prepares the organism to deal with threat (known as an emergency reaction): [[blood pressure]] and [[heart rate]] are increased, sweating is increased, bloodflow to the major muscle groups is increased, and [[immune system|immune]] and [[Digestion|digestive]] system functions are inhibited. Externally, somatic signs of anxiety may include pale skin, sweating, trembling, and [[mydriasis|pupillary dilation]]. Emotionally, anxiety causes a sense of dread or panic and physically causes nausea, and chills. Behaviorally, both voluntary and involuntary behaviors may arise directed at escaping or avoiding the source of anxiety and often maladaptive, being most extreme in [[anxiety disorder]]s. However, anxiety is not always pathological or maladaptive: it is a common emotion along with fear, anger, sadness, and happiness, and it has a very important function in relation to survival. | ||
Neural circuitry involving the [[amygdala]] and [[hippocampus]] is thought to underlie anxiety <ref>Rosen, J.B. & Schulkin, J. (1998): "From normal fear to pathological anxiety". ''Psychological Review''. '''105'''(2); 325-350.</ref>. When confronted with unpleasant and potentially harmful stimuli such as foul odors or tastes, [[Positron emission tomography|PET-scans]] show increased bloodflow in the amygdala <ref>Zald, D.H. & Pardo, J.V. (1997). "Emotion, olfaction, and the human amygdala: amygdala activation during aversive olfactory stimulation." ''Proc Nat'l Acad Sci'' USA. '''94'''(8), 4119-24.</ref> <ref>Zald, D.H., Hagen, M.C. & Pardo, J.V. (2002). "Neural correlates of tasting concentrated quinine and sugar solutions". ''J. Neurophysiol.'' '''87'''(2), 1068-75.</ref>. In these studies, the participants also reported moderate anxiety. This might indicate that anxiety is a protective mechanism designed to prevent the organism from engaging in potentially harmful behaviors. | Neural circuitry involving the [[amygdala]] and [[hippocampus]] is thought to underlie anxiety <ref>Rosen, J.B. & Schulkin, J. (1998): "From normal fear to pathological anxiety". ''Psychological Review''. '''105'''(2); 325-350.</ref>. When confronted with unpleasant and potentially harmful stimuli such as foul odors or tastes, [[Positron emission tomography|PET-scans]] show increased bloodflow in the amygdala <ref>Zald, D.H. & Pardo, J.V. (1997). "Emotion, olfaction, and the human amygdala: amygdala activation during aversive olfactory stimulation." ''Proc Nat'l Acad Sci'' USA. '''94'''(8), 4119-24.</ref> <ref>Zald, D.H., Hagen, M.C. & Pardo, J.V. (2002). "Neural correlates of tasting concentrated quinine and sugar solutions". ''J. Neurophysiol.'' '''87'''(2), 1068-75.</ref>. In these studies, the participants also reported moderate anxiety. This might indicate that anxiety is a protective mechanism designed to prevent the organism from engaging in potentially harmful behaviors. | ||
Revision as of 13:42, 20 December 2007
Stages of decompensation (psychology)
Distraction
This is a mental and emotional state where a person's attention is defocused because that individual is pre-occupied with a situation or set of feelings that are beyond their ability to manage in that moment.
Disorganization
Dysregulation
Dysfunction
Disorder
Dissociation
Intermittent explosive disorder
Intermittent explosive disorder (IED) is an Axis I impulse control disorder characterized by extreme expressions of anger, often to the point of uncontrollable rage, that are disproportionate to the situation at hand. [1] Impulsive aggression is unpremeditated, and is defined by a disproportionate reaction to any provocation, real or perceived. Some individuals have reported affective changes prior to an outburst (e.g., tension, mood changes, energy changes, etc.). [2]
A 2006 study published by Harvard University researchers suggests that the disorder is considerably more prevalent than previously thought. In a study of almost 10,000 individuals 18 years or older, lifetime episodes were reported at 7.3%, while 12-month occurrences were reported at 3.9%. This suggests a mean lifetime occurrence of 43 instances, with an average of $1359 in property damage. [3]
A 2005 study conducted in Rhode Island found the prevalence to be 6.3% (SE, +/- 0.7%) for lifetime DSM-IV IED in a study of 1300 patients under psychiatric evaluation. [4] The national prevalence has not been established,Template:Dubious and the disorder is considered to be relatively rare, due at least in part to the fact that an IED diagnosis is usually given only if all other possible disorders and syndromes are ruled out. Prevalence is higher in men than in women. [5] The disorder itself is not easily characterized and often exhibits comorbidity with other mood disorders, particularly bipolar disorder. [6]
In this same study, 27 subjects exhibiting DSM-IV IED were recruited and interviewed to describe their symptomology and episodic behaviors. All subjects described outbursts as brief, lasting an average of 22 minutes ± SD of 23 minutes. One-third of the subjects reported experiencing somatization prior to an episode, e.g. “tingling, tremor, palpitations, chest tightness, head pressure, or hearing an echo”. [6] Over half of the subjects reported an alteration in their awareness during the episode, but none reported amnesia of the outburst. Subjects generally reported an inability to resist the impulse to violence, and often reported a feeling of relief (88% reporting) or even pleasure (46% reporting) while committing the acts. After the acts, many subjects reported feelings of remorse at their actions. Remarkably, all 27 subjects reported their experiences with IED consistently.
Diagnosis & Treatment
The DSM-IV criteria for IED include: the occurrence of discrete episodes of failure to resist aggressive impulses that result in violent assault or destruction of property, the degree of aggressiveness expressed during an episode is grossly disproportionate to provocation or precipitating psychosocial stressor, and, as previously stated, diagnosis is made when other mental disorders that may cause violent outbursts (e.g., antisocial personality disorder, borderline personality disorder, attention deficit/hyperactivity disorder, etc.) have been ruled out.[6] Furthermore, the acts of aggression must not be due to a general medical condition, e.g., a head injury, Alzheimer’s disease, etc., or due to substance abuse or medication.[6] Diagnosis is made using a psychiatric interview to affective and behavioral symptoms to the criteria listed in the DSM-IV.
Treatment is achieved through both cognitive behavioral therapy and psychotropic medication regiments. Therapy aids in helping the patient recognize the impulses in hopes of achieving a level of awareness and control of the outbursts, along with treating the emotional stress that accompanies these episodes. Multiple drug regimens are frequently indicated for IED patients. Tricyclic antidepressants and serotonin reuptake inhibitors (SRIs) such as fluoxetine, fluvoxamine, and sertraline appear to alleviate some pathopsychological symptoms; the reasons for such will be explained further in the subsequent section. [7] GABAergic mood stabilizers and anticonvulsive drugs such as gabapentin, lithium, carbamazepine, and divalproex seem to aid in controlling the incidence of outbursts.[5] [8] Anxiolytics help alleviate tension and may help reduce explosive outbursts by increasing the provocative stimulus tolerance threshold, and are especially indicated in patients with comorbid obsessive-compulsive or other anxiety disorders.[5]
Pathophysiology
Impulsive behavior, and especially impulsive violence predisposition has been correlated to a low brain serotonin turnover rate, indicated by a low concentration of 5-hydroxyindoleacetic acid (5-HIAA) in the cerebral spinal fluid (CSF). This substrate appears to have important neurochemical properties, acting on the suprachiasmatic nucleus in the hypothalamus, which is the target for serotonergic output from the dorsal and median raphe nuclei. This site plays a role in the maintaining the circadian rhythm and regulation of glucose metabolism. A putative hereditary component to low CSF 5-HIAA and concordantly possibly to impulsive violence has been proposed upon observation that sons of alcoholic fathers who exhibit violent behavior also exhibit exceptionally low CSF 5-HIAA. Along with low CSF 5-HIAA concentration, vagal tone and increased insulin secretion has been observed in patients with confirmed DSM-IV IED.
Possible polymorphisms in the gene for tryptophan hydroxylase, which is responsible for the production of hydroxytryptophan, the precursor of serotonin. Within violent subjects, a significant relationship was observed between CSF 5-HIAA concentration and specific polymorphism genotypes. The phenotypes associated with these genotypes are extreme and it is hypothesized that these polymorphisms may only be significantly correlated to impulsive behavior. [9]
Additionally, lesions in the orbital/medial prefrontal cortex and related areas appear to be correlated to impulsively violent behavior, although currently no study has pinned down a specific area involved in IED. Research has shown, however, that damage in these areas, including the amygdale, increases the incidence of impulsive and aggressively violent behavior, and appears to decrease inhibition and ability to control emotion, as well as decreasing the ability to project consequences for their actions. Subjects who exhibit lesions in these regions may also exhibit decreased glucose metabolism, and concordantly decreased brain function in the prefrontal cortex, the region associated with decision making and action planning. More importantly is a reduced action in serotonergic neurons in this region as well as the amygdala. [10]
References
- ↑ American Psychiatric Association. (2000).''Diagnostic and Statistical Manual of Mental Disorders'' (4th ed.). Washington, DC: American Psychiatric Association.
- ↑ McElroy, S. L. (1999). Recognition and Treatment of DSM-IV Intermittent Explosive Disorder. J Clin Psychiatry, 60(suppl 15), 12-16.
- ↑ Kessler, R., Coccaro, E., Fava, M., Jaeger, S., Jin, R., Walters, E. (2006). The prevalence and correlates of DSM-IV intermittent explosive disorder in the national comorbidity survey replication. Archives of general psychiatry. Vol. 63.
- ↑ Coccaro, E. F., Posterkan, M. A., & Zimmerman, M. (2005). Prevalence and features of intermittent explosive disorder in a clinical setting. J Clin Psychiatry, 66(10), 1221-1227.
- ↑ 5.0 5.1 5.2 Boyd, M. A. (2005). Psychiatric nursing: contemporary practice (3rd ed.). Philadelphia: Lippincott Williams & Wilkins.
- ↑ 6.0 6.1 6.2 6.3 McElroy, S. L., Soutullo, C. A., Beckman, D. A., Taylor Jr., P., & Keck Jr., P. E. (1998). DSM-IV Intermittent Explosive Disorder: A report of 27 cases. J Clin Psychiatry, 59(4), 203-210.
- ↑ Goodman, W. K., Ward, H., Kablinger, A., & Murphy, T. (1997). Fluvoxamine in the Treatment of Obsessive-Compulsive Disorder and Related Conditions. J Clin Psychiatry, 58(suppl 5), 32-49.
- ↑ Bozikas, V., Bascilla, F., Yulis, P., & Savvidou, I. (2001). Gabapentin for Behavioral Dyscontrol with Mental Retardation. Am J Psychiatry, 158(6), 965.
- ↑ Virkkunen, M., Goldman, D., Nielsen, D. A., & Linnoila, M. (1995). Low Brain Serotonin Turnover Rate (Low CSF 5-HIAA) and Impulsive Violence. J Psychiatry Neurosci, 20(4), 271-275.
- ↑ Best, M., Williams, J. M., & Coccaro, E. F. (2002). Evidence for a dysfunctional prefrontal circuit in patients with an impulsive aggressive disorder. PNAS, 99(12), 8448-8453.
The Knights Templar
The Knights Templar or, more properly, The Order of the Poor Knights of Christ and the Temple of Solomon, were formed in the 1118, when nine pious knights arrived at the gates of Baldwin II, King of Jerusalem, and offered themselves as protectors of the faithful. They announced that they had taken the solemn vows of chastity, poverty, and obedience, as well as a fourth, perpetual vow to protect pilgrims on their journey from the coast to the Holy City of Jerusalem.
Anxiety
Anxiety is an elevated physiological state marked by demonstrable changes in cognitive, somatic, emotional, and behavioral components [1] These components combine to create the feelings that we typically recognize as fear, apprehension, or worry. Anxiety is often accompanied by physical sensations such as heart palpitations, nausea, chest pain, shortness of breath, stomach aches, or headache. The cognitive component entails expectation of a diffuse and certain danger. Somatically the body prepares the organism to deal with threat (known as an emergency reaction): blood pressure and heart rate are increased, sweating is increased, bloodflow to the major muscle groups is increased, and immune and digestive system functions are inhibited. Externally, somatic signs of anxiety may include pale skin, sweating, trembling, and pupillary dilation. Emotionally, anxiety causes a sense of dread or panic and physically causes nausea, and chills. Behaviorally, both voluntary and involuntary behaviors may arise directed at escaping or avoiding the source of anxiety and often maladaptive, being most extreme in anxiety disorders. However, anxiety is not always pathological or maladaptive: it is a common emotion along with fear, anger, sadness, and happiness, and it has a very important function in relation to survival.
Neural circuitry involving the amygdala and hippocampus is thought to underlie anxiety [2]. When confronted with unpleasant and potentially harmful stimuli such as foul odors or tastes, PET-scans show increased bloodflow in the amygdala [3] [4]. In these studies, the participants also reported moderate anxiety. This might indicate that anxiety is a protective mechanism designed to prevent the organism from engaging in potentially harmful behaviors.
- ↑ Seligman, M.E.P., Walker, E.F. & Rosenhan, D.L. (2001). Abnormal psychology, (4th ed.) New York: W.W. Norton & Company, Inc.
- ↑ Rosen, J.B. & Schulkin, J. (1998): "From normal fear to pathological anxiety". Psychological Review. 105(2); 325-350.
- ↑ Zald, D.H. & Pardo, J.V. (1997). "Emotion, olfaction, and the human amygdala: amygdala activation during aversive olfactory stimulation." Proc Nat'l Acad Sci USA. 94(8), 4119-24.
- ↑ Zald, D.H., Hagen, M.C. & Pardo, J.V. (2002). "Neural correlates of tasting concentrated quinine and sugar solutions". J. Neurophysiol. 87(2), 1068-75.