Showing posts with label PTSD. Show all posts
Showing posts with label PTSD. Show all posts

Saturday, 22 December 2012

Fear, a brief description


Fear is an emotion induced by a perceived threat that causes animals to move quickly away from the location of the perceived threat, and sometimes hide. It is a basic survival mechanism occurring in response to a specific stimulus, such as pain or the threat of danger. In short, fear is the ability to recognize danger leading to an urge to confront it or flee from it (also known as the fight-or-flight response) but in extreme cases of fear (horror and terror) a freeze or paralysis response is possible.

Fear is frequently related to the specific behaviors of escape and avoidance, whereas anxiety is the result of threats which are perceived to be uncontrollable or unavoidable. It is worth noting that fear almost always relates to future events, such as worsening of a situation, or continuation of a situation that is unacceptable. Fear can also be an instant reaction to something presently happening. All people have an instinctual response to potential danger, which is in fact important to the survival of all species. The reactions elicited from fear are seen through advantages in evolution. Fear can be a manipulating and controlling factor in an individuals life.
Some psychologists such as John B. Watson, Robert Plutchik, and Paul Ekman have suggested that there is only a small set of basic or innate emotions and that fear is one of them. This hypothesized set includes such emotions as joy, sadness, and anger. Fear should be distinguished from the emotion anxiety, which typically occurs without any certain or immediate external threat.
There are studies looking at areas of the brain that are affected in relation to fear. When looking at these areas (amygdala), it was proposed that a person learns to fear regardless of whether they themselves have experienced trauma, or if they have observed the fear in others. In a study completed by Andreas Olsson, Katherine I. Nearing and Elizabeth A. Phelps the amygdala were affected both when subjects observed someone else being submitted to an aversive event, knowing that the same treatment awaited themselves, and when subjects were subsequently placed in a fear-provoking situation. This suggests that fear can develop in both conditions, not just simply from personal history.
Although fear is learned, the capacity to fear is part of human nature. Because early humans that were quick to fear dangerous situations were more likely to survive and reproduce, preparedness is theorized to be a genetic effect that is the result of natural selection.
Other research showed that while the participants with the shorter version of the serotonin transporter gene developed a very strong physiological fear response to picture A, participants with a longer version of the gene did not. In addition, a variation in the gene coding for the COMT enzyme was associated with fear extinction volunteers with this particular variant were able to very quickly overcome their fear while volunteers with the other variant failed to do so.

Another study recently published in the Proceedings of the National Academy of Sciences claims to have found a link between a specific gene and the development of PTSD.
Dominique de Quervain of the University of Basel in Switzerland and his colleagues recruited around 700 healthy young volunteers, obtaining DNA samples from them to analyse the sequence of their PRKCA gene. This gene is one of many known to be involved in the formation of emotional memories, and encodes an enzyme called protein kinase C-α. The researchers then showed the participants a series of emotionally affecting photographs and shortly afterwards asked them to write down short descriptions of the images.
Participants carrying two copies of one variant within the PRKCA gene, dubbed the A allele, remembered the most details about the pictures. Those carrying two copies of the other variant  the G allele remembered the least, with the performance of those carrying one copy of each variant lying somewhere in the middle.
The researchers then asked 394 additional participants to perform the same task while undergoing brain imaging. This confirmed that variations in PKRCA are linked to the capacity for emotional memory, and further revealed that they were also associated with differences in brain activity during memory encoding. The task activated a large network of brain regions, including the hippocampus and amygdala, two structures in the medial temporal lobe that are known to be involved in memory formation and emotion, respectively.
The brain scans also showed that the A allele was associated with increased activity in the lateral and medial prefrontal cortex, regions that belong to a network involved in the encoding of emotional memories. Again, the increased activity in these areas was associated with the number of copies of the A allele carried by individuals people with two copies showed a larger increase in activity than those with just one.
Many researchers think that memory must have an important role in PTSD because traumatic memories are one of its core features, says de Quervain, “but it’s very hard to tell that a predisposition for building stronger memory is also a risk for developing the condition”.
“These findings are of considerable interest,” says neurobiologist James McGaugh of the University of California, Irvine. “It’s well established that emotional arousal enhances memory consolidation, and it’s widely assumed that this may contribute to PTSD, but the finding is important as it provides genetic evidence consistent with that hypothesis.”
The A allele is much more common in people of European than African descent, but exactly how this variation leads to differences in brain activity during the encoding of emotional memory is unclear. Large-scale genomic studies will probably uncover more gene variants associated with increased risk of developing PTSD
While genetic factors are helping us to find the causes of  PTSD, further study into early brain development may give us clues how Fear can influence our offspring.
Scientists have found that people with conservative views have brains with larger amygdalas, almond shaped areas in the centre of the brain often associated with anxiety and emotions.
The anterior cingulate is a part of the brain that is on the middle surface of the brain at the front and we found that the thickness of the grey matter, where the nerve cells of neurons are, was thicker the more people described themselves as liberal or left wing and thinner the more they described themselves as conservative or right wing. As the anterior cingulate is a higher functioning part of the brain which can allow intellectual reasoning.
While the amygdala is a part of the brain which is thought to be very primitive and functions as a basic emotions detector. The amygdala was larger in those people who described themselves as conservative. Studies in human children, on the other hand, found a connection between early social experiences and the volume of the amygdala, which helps regulate the processing and memory of emotional reactions. Numerous studies also have found that children raised in a nurturing environment typically do better in school and are more emotionally developed than their non-nurtured peers.
Brain images have now revealed that a mother’s love physically affects the volume of her child’s hippocampus.
In the study, children of nurturing mothers had hippocampal volumes 10 percent larger than children whose mothers were not as nurturing. Research has suggested a link between a larger hippocampus and better memory.
Its hard to figure out the potential fallout of a culture perpetuating fear and negative emotions, as each new born maybe effected by such factors. While small incidental moments of fear can be beneficial for recognizing dangers. A constant negative environment can potentially render people susceptible to PTSD as well as other factors on political views. The holistic interconnectivity explanation of fear as a never ending cycle maybe a scary thought. But considering it might perpetuate more fear I am likely to forget about the bad stuff and concentrate on a different emotion...



Monday, 5 November 2012

The Fear Factor, chemical bravery


Fear is an emotion induced by a perceived threat that causes animals to move quickly away from the location of the perceived threat, and sometimes hide. It is a basic survival mechanism occurring in response to a specific stimulus, such as pain or the threat of danger. In short, fear is the ability to recognize danger leading to an urge to confront it or flee from it (also known as the fight-or-flight response) but in extreme cases of fear (horror and terror) a freeze or paralysis response is possible.
The brain structure that is the center of most neurobiological events associated with fear is the amygdala, located behind the pituitary gland. The role of the amygdala in fear is best understood as part of a circuitry of fear learning. It is essential for proper adaptation to stress and specific modulation of emotional learning and memory. In the presence of a threatening stimulus, the amygdala generates the secretion of hormones that influence fear and aggression. Once response to the stimulus in the form of fear or aggression commences, the amygdala may elicit the release of hormones into the body to put the person into a state of alertness, in which they are ready to move, run, fight, etc. This defensive response is generally referred to in physiology as the fight-or-flight response regulated by the hypothalamus.

Exposure therapy is a behavioural therapy technique in which people with phobias, in a limited and structured manner, are exposed to their fears after being shown different relaxation and coping techniques, aimed at decreasing the intensity of their fear response. In a study, to prepare the participants for the exposure, they were given educational materials about exposure therapy and instructions on how to cope with their former avoidance strategies during the pre-treatment assessment. However, no cognitive behavioural techniques such as breathing or relaxation techniques were used.

Cortisol is a stress hormone released from the adrenal gland. It has many functions, including increasing blood sugar, but it is also thought to affect learning and memory processes. Cortisol is a type of hormone called a glucocorticoid. Previous animal research using other glucocorticoid hormones has shown them to be effective at promoting ‘extinction processes’ (lessening of fear during exposure to a fear-inducing stimulus). Therefore, the researchers wanted to see whether glucocorticoids could be useful in enhancing exposure therapy in humans.
The participants were given three sessions of exposure therapy using virtual exposure to heights. Virtual reality exposure to heights has been shown to be effective for treating people with acrophobia.
One hour before each session, half the participants were given a cortisol pill, while the other half were given a placebo pill. Neither the participants nor the person giving them the pills knew which pills were placebos. Three to five days after the last treatment session, the participants had a post-treatment session and were assessed once more a month later. These post-treatment assessments were compared to assessments made before the treatment had commenced. The success of the treatment was assessed by giving the participants questionnaires in which they were asked to rate how fearful they felt when considering 20 situations that could cause fear of heights.
This study shows that cortisol treatment prior to virtual reality exposure therapy sessions for acrophobia can have a beneficial effect compared to placebo with virtual reality exposure. The researchers also point out that virtual reality-based exposure therapy for fear of heights has been shown to be effective.
Alturnatively the Pentagon is spending up to $11 million at three medical research institutions with the hope that D-Cycloserine (DCS) can be used to get rid of fearful and horrific memories.
Experts at Emory University, the University of Southern California and New York-Presbyterian/Weill Cornell Medical Center will study the effectiveness of D-Cycloserine (DCS). DCS is a pharmaceutical thought to help extinguish fearful memories. It’s usually taken right before exposure therapy, a process that involves recalling traumatic experiences in an effort to nullify the menacing associations that accompany them.
Researchers will look at two different kinds of exposure therapy: Virtual reality, where a patient is fully immersed in digital combat scenarios, and prolonged imaginal exposure therapy, which asks them to simply remember and recount fearful memories. A total of 300 patients, all of them veterans from Iraq and Afghanistan, will partake. They’ll undergo seven individual weekly sessions of one of the therapies. Before each session, half will receive DCS, and the rest will get a placebo. Experts have already spent plenty of time figuring out how DCS works. It’s been around since the 1960s, when it was used to treat tuberculosis. Now, however, researchers are more excited about the drug’s potential ability to alleviate symptoms of depression, schizophrenia, obsessive-compulsive disorder and, of course, PTSD — without a lifetime of pill-popping.
DCS seems to enhance the brain’s learning process. For PTSD treatment, the drug could, ostensibly, help patients more quickly internalize that, say, driving down a suburban American highway is far different  and less dangerous than driving on a Baghdad street. The drug also binds to receptors in the amygdala, the region of the brain that governs fear response. So by blocking out fearful reactions while a patient revisits trauma, experts think DCS can, literally, “extinguish” fear right at the source. Emory researchers have already tried using DCS and virtual reality in humans with PTSD, fear of heights and obsessive compulsive disorder. Since 2006, Rothbaum and a team of experts have been comparing exposure therapy, used along with DCS, Xanax or placebo, in patients. “Results so far are positive,” Rothbaum says, though they haven’t finished analyzing the data.
That said, results from some other human studies on DCS aren’t encouraging. Several disappointing trials using DCS were presented by researchers assembled at the International Society for Traumatic Stress Studies conference. The Pentagon previously tried to treat PTSD with “illicit” substances, like marijuana and ecstasy, thus far have been cancelled.
The research team will also be conducting genetic tests on every patient. In particular, they’ll be looking at a gene dubbed “BDNF.” Experts already know that a variant of the BDNF gene can make fear extinction tougher. By comparing patient results to genes, Rothbaum says they hope to “figure out what’s the best treatment approach, and whether DCS can really rescue those patients, where maybe therapy alone can’t.” Of course, the idea of using drugs to tweak memories isn’t without controversy: An online debate flared last year among two camps of neurologists and neuroethicists, arguing over whether the existence of such drugs would “alter something that makes us all human”.
Then again, those debates hinge on DCS, or some other memory extinguisher, actually working. DCS’s efficacy is far from proven. And earlier research efforts that tested supposed “fear-extinguishing” drugs, most notably a series of much-touted, Pentagon-funded studies on Propanolol at Harvard, have all been disappointments.
Its still early days for a chemical pill to change our perception of what fear is, the danger is that the normal checks and balances that makes us safe could also change our personalities. Although it could be potentially useful in a combat situation or for Post traumatic syndrome . A chemical solution is not the best answer. But considering PTSD afflicts at least 250,000 of this generation’s soldiers, it might be helpful to find any solution at all...