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Zack Briones Group

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Trauma And Memory: Brain And Body In A Search F...

Preclinical and clinical studies have shown alterations in memory function following traumatic stress,53 as well as changes in a circuit of brain areas, including hippocampus, amygdala, and medial prefrontal cortex, that mediate alterations in memory.54 The hippocampus, a brain area involved in verbal declarative memory, is very sensitive to the effects of stress. Stress in animals is associated with damage to neurons in the CA3 region of the hippocampus (which may be mediated by hypercortisolemia, decreased brain-derived neurotrophic factor (BDNF), and/or elevated glutamate levels) and inhibition of neurogenesis.55-60 High levels of glucocorticoids seen with stress were also associated with deficits in new learning.61,62

Trauma and Memory: Brain and Body in a Search f...

Fewer brain imaging studies have been performed in children with PTSD. Several studies have shown alterations in electroencephalogram (EEG) measures of brain activity in children with a variety of traumas who were not selected for diagnosis compared with healthy children. About half of the children in these studies had a psychiatric diagnosis. Abnormalities were located in the anterior frontal cortex and temporal lobe and were localized to the left hemisphere.192,193 Two studies have found reductions in brain volume in children with trauma and PTSD symptoms.154,155 One group did not find reductions in hippocampal volume, either at baseline or over a longitudinal period,154,156 while another group found an 8.5% reduction in hippocampal volume that was not significant after controlling for smaller brain volumes in the PTSD group.155 One study used single-voxel proton magnetic resonance spectroscopy (proton MRS) to measure relative concentration of NAA and creatinine (a marker of neuronal viability) in the anterior cingulate of 11 children with maltreatment-related PTSD and 11 controls. The authors found a reduction in the ratio of NAA to creatinine in PTSD relative to controls.159 Studies have also found smaller size of the corpus callosum in children with abuse and PTSD relative to controls.154 as well as larger volume of the superior temporal gyrus.194 In a study of abused children in whom diagnosis was not specified, there was an increase in T2 relaxation time in the cerebellar vermis, suggesting dysfunction in this brain region.195 The reason for differences in findings between adults and children are not clear; however, factors such as chronicity of illness or interaction between trauma and development may explain findings to date.

Few studies have examined the effects of pharmacological treatment on brain structure and function in patients with trauma-related mental disorders. We studied a group of patients with depression and found no effect of fluoxetine on hippocampal volume, although there were increases in memory function230 and hippocampal activation measured with PET during a memory encoding task. Depressed patients with a history of childhood trauma were excluded, and we subsequently have found hippocampal volume reductions at baseline in women with early abuse and depression but not in women with depression without early abuse;198 this suggests that the study design of excluding patients with early trauma may account for the negative result. Other studies in depression showed that smaller hippocampal volume was a predictor of resistance to antidepressant treatment.231 Smaller orbitofrontal cortex volume is associated with depression; one study in geriatric depression found smaller orbitofrontal cortex volume, while length of antidepressant exposure was correlated with larger orbitofrontal volume.232

Body memory (BM) is a hypothesis that the body itself is capable of storing memories, as opposed to only the brain. While experiments have demonstrated the possibility of cellular memory[1] there are currently no known means by which tissues other than the brain would be capable of storing memories.[2][3]

Modern usage of BM tends to frame it exclusively in the context of traumatic memory and ways in which the body responds to recall of a memory. In this regard, it has become relevant in treatment for PTSD.[4]

Peter Levine calls BM implicit memory or more specifically procedural memory, things that the body is capable of doing automatically and not in one's consciousness. He clarifies 3 types of BM and frames his work in terms of traumatic memory consequence and resolution:[5]

A 2017 systematic review of cross-disciplinary research in body memory found that the available data neither largely support or refute the claim that memories are stored outside of the brain and more research is needed.[11]

Biologists at Tufts University have been able to train flatworms despite the loss of the brain and head. This may show memory stored in other parts of the body in some animals.[15] A worm reduced to 1/279th of the original can be regrown within a few weeks and be trained much quicker to head towards light and open space for food, an unnatural behavior for a flatworm. With each head removed training times appear reduced. This may just be a sign of epigenetics showing the appearance of memory.[16]

A traumatic brain injury (TBI) can be caused by a forceful bump, blow, or jolt to the head or body, or from an object that pierces the skull and enters the brain. Not all blows or jolts to the head result in a TBI.

Some injuries are considered primary, meaning the damage is immediate. Other outcomes of TBI can be secondary, meaning they can occur gradually over the course of hours, days, or appear weeks later. These secondary brain injuries are the result of reactive processes that occur after the initial head trauma.

Even after symptoms resolve entirely, people should return to their daily activities gradually once they are given permission by a doctor. There is no clear timeline for a safe return to normal activities although there are guidelines such as those from the American Academy of Neurology and the American Medical Society for Sports Medicine to help determine when athletes can return to practice or competition. Further research is needed to better understand the effects of mild TBI on the brain and to determine when it is safe to resume normal activities.

The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and use that knowledge to reduce the burden of neurological disease. NINDS, a component of NIH, supports research across the full range of TBI severity. Here is a list of efforts and developments.

Despite recent progress in understanding what happens in the brain following TBI, more than 30 large clinical trials have failed to identify specific treatments that make a dependable and measurable difference in people with TBI. A key challenge facing doctors and scientists is the fact that each person with a TBI has a unique set of circumstances based on such multiple variables as the location and severity of the injury, the person's age and overall heath, and the time between the injury and the initiation of treatment. These factors, along with differences in care across treatment centers, highlight the importance of coordinating research efforts so that the results of potential new treatments can be confidently measured.

People with a TBI also can support TBI research by designating the donation of brain tissue before they die. The study of human brain tissue is essential to increasing the understanding of how the nervous system functions.

The NIH NeuroBioBank is an effort to coordinate the network of brain banks it supports across the country to advance research through the collection and distribution of post-mortem brain tissue. Stakeholder groups include brain and tissue repositories, researchers, NIH program staff, information technology experts, disease advocacy groups, and most importantly individuals seeking information about opportunities to donate. It ensures protection of the privacy and wishes of donors.

Fibromyalgia is a disorder characterized by widespread musculoskeletal pain accompanied by fatigue, sleep, memory and mood issues. Researchers believe that fibromyalgia amplifies painful sensations by affecting the way your brain and spinal cord process painful and nonpainful signals.

Many researchers believe that repeated nerve stimulation causes the brain and spinal cord of people with fibromyalgia to change. This change involves an abnormal increase in levels of certain chemicals in the brain that signal pain.

A literature search was conducted to identify fMRI, PET and SPECT studies of symptom provocation in traumatized individuals. The search for neuroimaging data was conducted on Medline, PubMed and Psychinfo in mid-January 2012. The search terms were: PTSD or ASD (acute stress disorder) + symptom provocation + PET (positron emission tomography), SPECT (single photon emission computerized tomography) or fMRI (functional magnetic resonance imaging). In addition, the reference lists of resulting articles were reviewed for relevant studies not identified by the initial database search. The search yielded 24 studies from which a subset was selected according to the following inclusion criteria: (1) PTSD or ASD diagnosis in the patient group, (2) symptom provocation, i.e., the use of trauma-related stimuli and a control condition.

The coordinate-based meta-analysis of neural activation during trauma-related stimulation partly confirms and partly contradicts the current model of brain circuitry of PTSD. Furthermore, important additional areas were shown to be activated that hitherto have been neglected in the modeling of trauma symptoms. In patients, results from the between group and between condition analyses were widely overlapping.

Among the limitations of this meta-analysis is the relatively small sample size of most of the studies included and their heterogeneity of the symptom provocation methods. Furthermore, additional analyses using control volunteers who had not undergone the traumatic event could have been informative in differentiating reactions to stimulus salience from autobiographical memory. However, as yet there are not enough studies involving unconcerned controls. Finally, heterogeneity among studies resulted from some of them reporting whole-brain analysis and others region-of-interest analysis. We hoped to compensate at least partly for the heterogeneity by using a random-effects model. 041b061a72

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