Posts Tagged Amygdala
Post by D. Chloe Chung
“I was so anxious to do what is right that I forgot to do what is right.” – Jane Austin
What’s the deal with anxiety?
You’re giving an important presentation tomorrow for work in front of a big crowd. You know you’re well-prepared, but when you imagine yourself standing at the podium, facing strangers whose eyes are fixed on you, you start to feel nauseated – your palms sweat and your heart hammers in your chest. You’re experiencing acute anxiety, a state of negative emotions and heightened arousal, often accompanied by increased alertness. This definition may sound similar to that of ‘fear’, which is produced as an acute response to immediate threats. There is considerable overlap between the brain circuitry regulating anxiety and fear, but anxiety is distinct from fear because it can be internally triggered or anticipatory – just like when you were merely imagining that presentation for work. Much of our understanding of anxiety stems from what we have learned about how the brain processes and learns fear responses.
What’s going on in your brain when you’re feeling anxious?
Recent research efforts have emphasized the importance of communication between multiple brain areas in evoking anxiety. One of the established models of the neural circuitry of anxiety proposes that anxiety arises due to active neural communication between brain regions, including the amygdala, a brain structure involved in fear learning. The amygdala (the central extended amygdala [CeA]) sends projections to the bed nucleus of the stria terminalis (BNST), a cluster of nuclei involved in threat monitoring. The amygdala and the BNST also communicate with other brain regions such as the ventral hippocampus (vHPC) and the prefrontal cortex (PFC). According to this model, these four regions are connected by neural projections and work with one another in an orchestrated manner to evaluate whether or not a situation is threatening. The brain activity in this group of regions that we’ll refer to as the ‘anxiety detection’ regions can be either anxiogenic or anxiolytic, meaning they can perpetuate or reduce anxiety, respectively.
Downstream, the motor cortex, regions of the brainstem, and the neuroendocrine system receive, interpret, and evaluate possible anxiety signals from the brain regions involved in anxiety detection. These downstream regions then initiate anxiety responses by triggering defensive and risk-avoiding behaviors and altering biological functions such as heart and respiration rate. Excessive anxiety can occur when the brain’s anxiety pathways misinterpret incoming signals. For instance, repeated exposure to ‘threatening’ situations may cause anxiogenic pathways to become abnormally hyperactive, and therefore more sensitive to threatening stimuli. This can cause an imbalance in the neural circuitry that processes anxiety, shaping the brain to become more reactive and susceptible to experiencing anxiety.
What’s new in anxiety research?
While we know the amygdala (specifically the CeA) is particularly important for anxiety regulation, the exact mechanisms are difficult to disentangle. Recent research has helped to shed light on some of the specific circuitry involved. A recent study in the Journal of Neuroscience used a novel rat model and deleted a gene called ErbB4 – implicated in various neurological disorders – in a group of amygdala neurons that release somatostatin, a peptide implicated in fear responses. In behavioral tests, rats without this gene exhibited higher anxiety levels, due to increased somatostatin levels in the amygdala. The abnormal activity of somatostatin neurons in the CeA also disrupted the inhibition of somatostatin neurons in the BNST, rendering these neurons hyperactive and ultimately causing heightened anxiety. A peptide called dynorphin has been identified as a key molecular player in this amygdala-BNST anxiety circuit. The authors demonstrated that the amount of dynorphin produced by somatostatin neurons in the amygdala was increased, and led to disinhibition of the BNST, contributing to the induction of anxiety-related behaviors. In other words, both somatostatin and dynorphin work together to play an important role in increased anxiety in mice without ErbB4. The good news is that dynorphin could be a potential target for anxiety treatment.
Another area of anxiety research concerns the stress neuropeptide, corticotropin-releasing factor. It’s known to regulate the BNST’s ability to elicit anxiety, but it was unclear where the corticotropin-releasing factor was coming from until recently. A study published by Pomrenze et al. showed that corticotropin-releasing factor is majorly produced and released by a group of neurons located in the lateral amygdala and the dorsolateral BNST. Using designer drugs that can either inhibit or activate neurons expressing the corresponding receptors via viral transduction, the authors found that neurons that project from the lateral amygdala to the BNST and release corticotropin-releasing factor are critical in mediating anxiety. Removal of these neurons reduced anxiety behaviors, confirming the importance of corticotropin-releasing factor in evoking anxiety responses.
What happens when anxiety interferes with daily life?
Modern life is full of stressors and many people are prone to experiencing intense anxiety at some point in their lives. In fact, anxiety is a part of a normal emotional spectrum and can even be beneficial at times, increasing our vigilance and enabling our survival. However, chronic anxiety can severely interfere with day-to-day living and become pathological, resulting in generalized anxiety disorder (GAD) or other anxiety-related disorders. Anxiety disorders like GAD are common, impacting one in every five adults. Considering how many individuals are affected by pathological anxiety, there is a need for highly effective anti-anxiety drugs or behavioral interventions. It is critical to understand the brain circuitry underlying anxiety to develop effective treatment options for chronic anxiety disorders.
Since anxiety results in heightened arousal, many anxiety medications manipulate neurotransmitters to slow the nervous system down, decreasing arousal. Medications such as selective serotonin reuptake inhibitors (SSRIs) and Buspirone work to increase serotonin in the nervous system, which can, in turn, decrease arousal. Medication options for phobias such as social anxiety tend to decrease the effect of norepinephrine, a neurotransmitter connected to the ‘fight or flight’ fear response. Cognitive-behavioral therapy (CBT) and consulting with certified therapists can also improve anxiety. CBT is a popular and effective strategy that guides individuals to replace anxiety-provoking interpretations of situations with benign ones. For individuals with less severe anxiety symptoms, CBT can sometimes work as well as some medications, depending on the person and the extent of their anxiety. CBT can also be combined with other therapeutic approaches to effectively treat anxiety depending on the severity of symptoms. Regular physical exercise and breathing exercises can also be effective in reducing anxiety symptoms.
Things to remember about anxiety
To manage acute daily anxieties, remembering how the brain circuitry of anxiety works might be helpful – the anxiety regions of the brain first assess whether the situation is threatening or not, and then subsequently trigger the anxiety response. This means that we can practice psychological tricks to aid the brain in better assessing non-threatening situations as just that – non-threatening. Similar to CBT, by taking a step back and evaluating the situation, we can develop habits that lead to new responses and potentially avoid an unnecessary anxiety response in the future. Making an effort to be aware of our anxious thoughts or worries and replacing them with more realistic ones can also be beneficial in helping our brain to relearn our responses to potentially threatening situations. Since the human brain is plastic (i.e. it adapts to changes in our internal and external environments), conscious efforts can result in a shift in the anxiety circuitry. Another key factor in mitigating anxiety is an awareness of the surrounding environment. Anxiety-inducing neural circuitry can be over-activated when we’re repeatedly exposed to certain stressors in our environment, resulting in feelings of anxiety in situations that are not immediately threatening. Hence, eliminating or minimizing such stressors in our environment can help.
Calhoon GG, Tye KM. Resolving the neural circuits of anxiety. Nature Neuroscience (2015) 18(10): 1394-404. DOI: 10.1038/nn.4101.
Ahrens S, Wu MV, Furlan A, Hwang GR, Paik R, Li H, Penzo MA, Tollkuhn J and Li B. A central extended amygdala circuit that modulates anxiety. Journal of Neuroscience (2018) 38(24): 5567-5583. DOI: 10.1523/JNEUROSCI.0705-18.2018
Pomrenze MB, Tovar-Diaz J, Blasio A, Maiya R, Giovanetti SM, Lei K, Morikawa H, Hopf FW and Messing RO. A corticotropin releasing factor network in the extended amygdala for anxiety. Journal of Neuroscience (2019) 39(6): 1030-1043. DOI: 10.1523/JNEUROSCI.2143-18.2018
Hofmann SG, Asnaani A, Vonk IJJ, Sawyer AT, and Fang A. The Efficacy of Cognitive Behavioral Therapy: A Review of Meta-analyses. Cognitive Therapy and Research (2012) 36(5): 427-440. DOI: 10.1007/s10608-012-9476-1
Kaczkurkin AN, Foa EB. Cognitive-behavioral therapy for anxiety disorders: an update on the empirical evidence. Dialogues in Cinical Neuroscience (2015) 17(3):337-46. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4610618/
Neuroscience findings suggest that psychotherapy alters the brain.
Since the decade of the brain, 1990-1999, neuroscience has captured enormous amounts of attention from both the scientific community and the general public. Many books and media reports describe the brain’s basic anatomy and function. There has been a proliferation of neuroscience institutes at universities. In laboratories all over the world, neuroscience has become one of the most exciting and productive branches of inquiry.
Yet not everyone is completely pleased with what neuroscience has to tell us. In particular, some decry neuroscience for trying to delegitimize the “mind.” Going back to the original Cartesian mind-body duality, these critics insist that neuroscience can only go so far by describing the function of neurons and neurotransmitters. What cannot be reached by science, they say, is that ineffable “mind” that constitutes the human spirit. For them, neuroscience is purely an attempt to reduce the complexities and wonders of human experience to brain scan images and electrical recordings from axons and dendrites.
In a new book, Neuroscience at the Intersection of Mind and Brain (Oxford University Press, 2018), one of us (Jack) attempts to allay fears that neuroscience will somehow reduce human experience and creativity to the “mere” workings of the physical brain. There is, in fact, nothing “reductive” about the physical brain. Rather, the brain is a gloriously complex, fascinating, and well-organized structure that constitutes, as neuroscientist Eric Kandel so eloquently put it, “the organ of the mind.”
Biologists versus Psychologists
As a resident in psychiatry in the late 1970s, Jack witnessed the emergence of psychopharmacology as the dominant discipline for academic psychiatry and lived through the often bitter battles between “biologists” and “psychologists.” This may be, in part, where the mistrust of neuroscience began. The biologists believed that their method of treating psychiatric illness—medication—was based on solid science and rejected psychotherapy as unscientific. They also believed that neuroscience explained why the new psychiatric drugs worked and therefore promoted brain science as the basis for their discipline. Every lecture about depression or schizophrenia in those days began with a picture of a pre- and postsynaptic neuron forming a synapse across which neurotransmitters like serotonin, noradrenaline, and dopamine carried information. The new medications interact with receptors for these neurotransmitters and, it was taught at the time, this explains how they work to treat depression, anxiety, and psychosis.
It turns out that the picture of neurons everyone used back then was a vast oversimplification of what a synapse really looks like and that almost nothing we know about neurotransmitters and their receptors actually explains how psychiatric drugs work. But what really bothered the psychologists was the complete dismissal of psychotherapy by the biologists. Years of studying various types of psychotherapy convinced them that indeed they had science on their side. Furthermore, they objected to the biologists’ emphasis on inherited abnormalities as the sole basis for psychiatric illness. Psychologists had always been more interested in the ways that human experience, from birth onwards, shaped personality and behavior.
Over time, many (but thankfully not all) psychologists came to see neuroscience as the branch of science devoted to promoting pharmacology as the only treatment for psychiatric illness and to trying to prove that those illnesses were entirely due to inherited brain abnormalities. Biologists stood with nature; psychologists with nurture.
This fear of neuroscience’s aims is entirely misplaced. Over the last several decades, neuroscience has, in fact, focused a great deal of attention on the biology of experience, elucidating the ways in which what happens to us in life affects the structure and function of the brain. Every time we see, hear, smell, or touch something, learn a new fact, or have a new experience, genes are activated in the brain, new proteins are synthesized, and neural pathways communicate the new information to multiple brain regions.
Neuroscience is not, therefore, synonymous with psychopharmacology, nor does it invalidate the complexities of human experience. It has shown, for example, that early life interactions between a parent and child shape how the brain will function for the rest of a person’s life.
This has tremendous implications for understanding the mechanism of action of psychotherapy if we accept the idea that psychotherapy itself is a form of life experience and therefore capable of changing brain function at molecular, cellular, and structural levels. Here are two examples that illustrate ways in which neuroscience informs psychotherapy.
CBT and the Prefrontal to Amygdala Connection
It is now clear that the expression of conditioned fear is dependent upon an intact, functioning amygdala. Scientists have shown that the amygdala, located in a primitive part of the brain often referred to as the limbic cortex, reciprocally inhibits and is inhibited by a more evolutionarily advanced part of the brain, the medial prefrontal cortex (mPFC). Thus, under circumstances of heightened fear, the amygdala shuts down the ability of the mPFC to exert reason over emotion and initiates a cascade of fearful responses that include increased heart rate and blood pressure and freezing in place. When the mPFC is able to reassert its capacity for logic and reason, it can, in turn, inhibit the amygdala and reduce and extinguish fear.
Cognitive behavioral therapy (CBT) is an evidence-based intervention that is the first-line treatment for most anxiety disorders and for mild, moderate, and in many cases even severe depression. Because the automatic, irrational fears and avoidance behaviors manifested by patients with anxiety disorders and depression resemble the behavior of rodents in Pavlovian fear conditioning experiments, scientists have wondered if CBT works, at least in part, by strengthening the prefrontal cortex to amygdala pathway, thereby reducing amygdala activity. Indeed, many studies have shown that anxious and depressed patients have reduced activity in this pathway and exaggerated amygdala responses to fearful stimuli. Studies have also shown that successful CBT for social anxiety disorder decreases amygdala activation.
Most recently, a group of scientists from Oxford, Harvard, and Berkeley showed clearly that stimulation of the prefrontal cortex in human volunteers both reduced amygdala activation and fear. Maria Ironside and colleagues selected 18 women with high levels of trait anxiety and randomized them to receive either transcranial direct current stimulation (tDCS) to the prefrontal cortex or sham tDCS. The subjects underwent functional magnetic resonance imaging (fMRI) of the brain and performed an attentional load task that tests vigilance to threat. Real, but not sham, tDCS increased activity in the prefrontal cortex, decreased activity in the amygdala, and decreased threat responses.
This study is one example of preclinical and clinical neuroscience coming together to suggest a biological mechanism for the efficacy of a psychosocial intervention. We know that the cognitive portion of CBT strengthens a patient’s ability to assert reason over irrational thoughts and fears and that this decreases amygdala activity in some studies. We know clearly from animal studies that stimulating the prefrontal cortex reduces amygdala activation and potentiates fear extinction. Now we also know that in a group of anxious people, direct stimulation of the prefrontal cortex does exactly the same thing as it does in animal studies and, in addition, reduces anxiety. With this plausible hypothesis for how CBT works, scientists can now push further to see if brain imaging can ultimately help select patients with particularly weak prefrontal to amygdala pathway strength who might be prime candidates for CBT and then to track how they are doing in therapy objectively by repeating the brain imaging studies to see if and when that pathway is strengthened.
Psychoanalysis and Reconsolidation
CBT has been proven effective by many high-quality clinical trials and therefore is a prime candidate for biological studies, but can the same be said for such widely used but not empirically-validated treatments as psychoanalysis and psychoanalytic psychotherapy? In 2011, Jack and his colleague, Columbia psychiatrist and psychoanalyst Steven Roose, proposed that another aspect of fear conditioning—reconsolidation of fear memories—may explain one biological mechanism of action for how psychoanalysis works. In rats, when a conditioned fear memory is reactivated, it temporarily becomes labile and can be completely erased by blocking the biological mechanisms that permit reconsolidation of the memory. Could it be that in psychoanalytic therapies, the patient undergoes a process of reactivating distressing early memories that, once made conscious through the psychoanalytic process, can be manipulated by the therapist’s interpretations? According to this hypothesis, those now altered memories can then be reconsolidated into permanent memory in a less disturbing format.
The theory has been considered since then by many scientists and psychoanalytic theorists and a number of experiments show that the phenomena of labile reactivated memories and blockade of reconsolidation do indeed occur in humans. Blocking reconsolidation of reactivated memories has been shown to be effective in experiments attempting to help addicts overcome the powerful tendency to succumb to subtle cues and resume taking drugs even after successful rehabilitation. Here again, information gained from the basic neuroscience laboratory and from clinical neuroscience studies may help us understand how one aspect of psychoanalysis works to change the brain in ways that are helpful to people suffering with mental illness.
It is not necessary to invoke an ineffable “mind” to explain our unique human characteristics. Understanding the complexity of the human brain is sufficient to reveal how we are able to take what we experience and transform it into scientific theories, poetry, and philosophical ideas. Neuroscience is not superficial or reductionistic and it is not at all in the sole service of psychopharmacology and the genetic explanation for mental disorders. This becomes clear as we recognize the tremendous contributions neuroscientists have made to elucidating basic mechanisms that allow experiences to change the physical structure and function of the brain on a second-by-second basis. Everything we experience during life is translated into events that occur in the brain.
Psychotherapy is a form of life experience that changes the way the brain works, often ameliorating abnormalities caused by adverse experience and stressful life events. So yes, there is a science to psychotherapy, one that can be readily understood by learning about some of the fundamental and fascinating ways our brains work. Neuroscience at the Intersection of Mind and Brain tries to do just that.
An international research consortium used neuroimaging techniques to analyze the brains of more than 3,800 volunteers in different countries. The largest study of its kind ever conducted set out to investigate anatomical similarities and differences in the brains of individuals with different types of epilepsy and to seek markers that could help with prognosis and treatment.
Epilepsy’s seizure frequency and severity, as well as the patient’s response to drug therapy, vary with the part of the brain affected and other poorly understood factors. Data from the scientific literature suggests that roughly one-third of patients do not respond well to anti-epileptic drugs. Research has shown that these individuals are more likely to develop cognitive and behavioral impairments over the years.
The new study was conducted by a specific working group within an international consortium called ENIGMA, short for Enhancing NeuroImaging Genetics through Meta-Analysis, established to investigate several neurological and psychiatric diseases. Twenty-four cross-sectional samples from 14 countries were included in the epilepsy study.
Altogether, the study included data for 2,149 people with epilepsy and 1,727 healthy control subjects (with no neurological or psychiatric disorders). The Brazilian Research Institute for Neuroscience and Neurotechnology (BRAINN), which participated in the multicenter study, was the center with the largest sample, comprising 291 patients and 398 controls. Hosted in Brazil, at the State University of Campinas (UNICAMP), BRAINN is a Research, Innovation and Dissemination Center (RIDC http://cepid.fapesp.br/en/home/) supported by the Sao Paulo Research Foundation – FAPESP.
“Each center was responsible for collecting and analyzing data on its own patients. All the material was then sent to the University of Southern California’s Imaging Genetics Center in the US, which consolidated the results and performed a meta-analysis,” said Fernando Cendes, a professor at UNICAMP and coordinator of BRAINN.
A differential study
All volunteers were subjected to MRI scans. According to Cendes, a specific protocol was used to acquire three-dimensional images. “This permitted image post-processing with the aid of computer software, which segmented the images into thousands of anatomical points for individual assessment and comparison,” he said.
According to the researcher, advances in neuroimaging techniques have enabled the detection of structural alterations in the brains of people with epilepsy that hadn’t been noticed previously.
Cendes also highlighted that this is the first epilepsy study built on a really large number of patients, which allowed researchers to obtain more robust data. “There were many discrepancies in earlier studies, which comprised a few dozen or hundred volunteers.”
The patients included in the study were divided into four subgroups: mesial temporal lobe epilepsy (MTLE) with left hippocampal sclerosis, MTLE with right hippocampal sclerosis, idiopathic (genetic) generalized epilepsy, and a fourth group comprising various less common subtypes of the disease.
The analysis covered both patients who had had epilepsy for years and patients who had been diagnosed recently. According to Cendes, the analysis – whose results were published in the international journal Brain – aimed at the identification of atrophied brain regions in which the cortical thickness was smaller than in the control group.
The researchers first analyzed data from the four patient subgroups as a whole and compared them with the controls to determine whether there were anatomical alterations common to all forms of epilepsy. “We found that all four subgroups displayed atrophy in areas of the sensitive-motor cortex and also in some parts of the frontal lobe,” Cendes said.
“Ordinary MRI scans don’t show anatomical alterations in cases of genetic generalized epilepsy,” Cendes said. “One of the goals of this study was to confirm whether areas of atrophy also occur in these patients. We found that they do.”
This finding, he added, shows that in the case of MTLE, there are alterations in regions other than those in which seizures are produced (the hippocampus, parahippocampus, and amygdala). Brain impairment is, therefore, more extensive than previously thought.
Cendes also noted that a larger proportion of the brain was compromised in patients who had had the disease for longer. “This reinforces the hypothesis that more brain regions atrophy and more cognitive impairment occurs as the disease progresses.”
The next step was a separate analysis of each patient subgroup in search of alterations that characterize each form of the disease. The findings confirmed, for example, that MTLE with left hippocampal sclerosis is associated with alterations in different neuronal circuits from those associated with MTLE with right hippocampal sclerosis.
“Temporal lobe epilepsy occurs in a specific brain region and is therefore termed a focal form of the disease. It’s also the most common treatment-refractory subtype of epilepsy in adults,” Cendes said. “We know it has different and more severe effects when it involves the left hemisphere than the right. They’re different diseases.”
“These two forms of the disease are not mere mirror-images of each other,” he said. “When the left hemisphere is involved, the seizures are more intense and diffuse. It used to be thought that this happened because the left hemisphere is dominant for language, but this doesn’t appear to be the only reason. Somehow, it’s more vulnerable than the right hemisphere.”
In the GGE group, the researchers observed atrophy in the thalamus, a central deep-lying brain region above the hypothalamus, and in the motor cortex. “These are subtle alterations but were observed in patients with epilepsy and not in the controls,” Cendes said.
Genetic generalized epilepsies (GGEs) may involve all brain regions but can usually be controlled by drugs and are less damaging to patients.
From the vantage point of the coordinator for the FAPESP-funded center, the findings published in the article will benefit research in the area and will also have future implications for the diagnosis of the disease. In parallel with their anatomical analysis, the group is also evaluating genetic alterations that may explain certain hereditary patterns in brain atrophy. The results of this genetic analysis will be published soon.
“If we know there are more or less specific signatures of the different epileptic subtypes, instead of looking for alterations everywhere in the brain, we can focus on suspect regions, reducing cost, saving time and bolstering the statistical power of the analysis. Next, we’ll be able to correlate these alterations with cognitive and behavioral dysfunction,” Cendes said.
[BLOG POST] From Ken Collins: When we injure our brain, we injure an important part of our body. – Broken Brain – Brilliant Mind
When we injure our brain, we injure an important part of our body. Our brains control our ability to think, talk, move, and breathe. In addition to being responsible for our senses, emotions, memory, and personality, our brain allows every part of our body to function even when we’re sleeping.
The brain can be hijacked by the Amygdala in the limbic system after our brain injuries as outlined in this source:
Wikipedia: Daniel Goleman speaks about Amygdala hiijacking – Amygdala hijack is a term coined by Daniel Goleman in his 1996 book Emotional Intelligence: Why It Can Matter More Than IQ. Drawing on the work of Joseph E. LeDoux, Goleman uses the term to describe emotional responses from people which are immediate and overwhelming, and out of measure with the actual stimulus because it has triggered a much more significant emotional threat. From the thalamus, a part of the stimulus goes directly to the amygdala while another part is sent to the neocortex or “thinking brain”. If the amygdala perceives a match to the stimulus, i.e., if the record of experiences in the hippocampus tells the amygdala that it is a fight, flight or freeze situation, then the amygdala triggers the HPA (hypothalamic-pituitary-adrenal) axis and hijacks the rational brain. This emotional brain activity processes information milliseconds earlier than the rational brain, so in case of a match, the amygdala acts before any possible direction from the neocortex can be received. If, however, the amygdala does not find any match to the stimulus received with its recorded threatening situations, then it acts according to the directions received from the neo-cortex. When the amygdala perceives a threat, it can lead that person to react irrationally and destructively.
Goleman states that “[e]motions make us pay attention right now — this is urgent – and gives us an immediate action plan without having to think twice. The emotional component evolved very early: Do I eat it, or does it eat me?” The emotional response “can take over the rest of the brain in a millisecond if threatened.”HYPERLINK “http://en.wikipedia.org/wiki/Amygdala_hijack”%5B5%5D An amygdala hijack exhibits three signs: strong emotional reaction, sudden onset, and post-episode realization if the reaction was inappropriate.
Goleman later emphasized that “self-control is crucial …when facing someone who is in the throes of an amygdala hijack” so as to avoid a complementary hijacking – whether in work situations, or in private life. Thus for example ‘one key marital competence is for partners to learn to soothe their own distressed feelings…nothing gets resolved positively when husband or wife is in the midst of an emotional hijacking.' The danger is that “when our partner becomes, in effect, our enemy, we are in the grip of an ‘amygdala hijack’ in which our emotional memory, lodged in the limbic center of our brain, rules our reactions without the benefit of logic or reason…which causes our bodies to go into a ‘fight or flight’ response.”.
Understanding the role stress plays on triggering the limbic system fight or flight response is critical for people to learn about after our brain injuries. Brain injuries are often described as either traumatic or acquired based on the cause of the injury.
Traumatic brain injury (TBI) is an insult to the brain, not of a degenerative or congenital nature, which is caused by an external physical force that may produce a diminished or altered state of consciousness, and results in an impairment of cognitive abilities or physical functioning. It can also result in the disturbance of behavioral or emotional functioning.
A TBI can affect our ability to, think and solve problems, move our body and speak, and control our behavior, emotions, and reactions.
Acquired brain injuries are caused by many medical conditions, including strokes, encephalitis, aneurysms, anoxia (lack of oxygen during surgery, drug overdose, or near drowning), metabolic disorders, meningitis, and brain tumors.
Although the causes of brain injury differs, the effects of these injuries on a person’s life are quite similar.
This is why understanding about the consequences of stress on the limbic system after a brain injury is so important.
Understanding the Sympathetic Nervous System in the brain injury recovery process is seldom talked about to us after our brain injuries by doctors or health care professionals because they only treat the symptoms.
The following information is critical to understand and has great value for people with brain injuries and their families to understand.
The Sympathetic Nervous System – “limbic system is autonomic” and creates many problems people with brain injuries face during our recovery process. If people with brain injuries don’t understand the Sympathetic Nervous System and how it works – our family members and friends react to our emotions and unwittingly create more stress for us for us to deal with.
This stress triggers the “limbic system’s fight or flight response” into action.
We do not have any control over what we are reacting to because of the stress that is being generated by our emotions shuts down the thinking part of our brain – pre-frontal cortex.
What happens next is – we react and they react, the stress builds and we lose control, get angry and have emotional meltdowns or worse.
During any stressful situation our loved ones react to our “actions” and we react to theirs – which increases our stress during those hard and difficult times.
We (family members/ people with brain injuries and friends) get caught up in a reactionary mode instead of being proactive to keep the limbic system in check.
If we set up daily routines, have structure and find purpose and meaning in our lives we have a better chance of controlling stress and the situations that trigger the limbic system fight or flight response.
If we do not control the stress, our families and friends will constantly be reacting to issues we have little control over. Learning relaxation techniques like mindfulness-based stress reduction can help to stay calm so the limbic system is managed.
Mindfulness-based stress reduction can help with this and I encourage you to look this up on the internet because there is a lot to learn about this tool that can help us rebuild or lives after a brain injury.
After our brain injuries “emotional outbursts, anger, and memory issues” are an expression of the problems caused by our limbic system fight or flight response under stress. By understanding how our emotions can get out of control we will have a better understanding of why we react to things that don’t make any sense to us.
There is a reason for all this madness and by learning the role the sympathetic nervous system plays in our recovery, the better chance we have to live full and rewarding lives again – after our brain injuries!