Questions related to Traumatic Brain Injury
What have we seen that is helping patients with Traumatic brain injuries and Acquired Brain Injuries to assist them in their rehabilitation, particularly long term patients? What evidence of successes are there and how can we use them to assist outpatients
1. I would like to know the material coefficient names called for MU1, MU2, A1, A2, Incompressibility Parameters D1 and D2 in ANSYS .
Secondly, I wanted any papers which gives the brain and skull material properties where I can find these Ogden 2nd order values.
Ignroant question - for RAT brain tissue.
I have been looking at how the GABA receptor is affected by traumatic brain injury and there is a good couple of papers saying that the subunits change in the GABA-A and GABA-B after injury.
My scientific question being: Do the subunits of the GABA receptors change after injury? (i have numerous time points)
I was hoping to stain with my interneuronal stains for Parvalbumin and Somatostatin (separately) and also GABA subunits. Maybe that is stupid ..
Looking briefly at some lit. and it says for GABA-A that alpa1 and Y2 are affected and change.
I have seen some antibodies for these subunits and a couple of papers stain for these subunits. But from what I can see the masses check the expression from western blots and not 'cell' density using immunohistochemistry.
Some do both so show where the decrease of expression is likely from - (very severe tbi in the rat brain) so was clear where the loss was. My TBI is much milder and diffuse.. so i am worried wouldn't see anything..
What is the best way to go about this?
I feel like it is western blots, but I am delving into a new area here and looking for some validation or maybe someone to point out something very obvious...
I am doing a systematic review and meta-analysis looking at predictors of PTSD symptoms after traumatic brain injury. Some of the studies I have included are analyses of subsets of participants within the same larger prospective cohort study. For example, the papers may explore different potential predictors of PTSD.
I imagine there will be considerable overlap in the participants analysed in each paper, considering that they're coming from the same larger cohort study. However, am I able to still include multiple of these papers given that they're investigating different predictors? Or do I just have to pick the one most comprehensive paper for inclusion? It would seem like a real shame to exclude all papers but one as it would leave out some novel and good-quality findings.
Any advice would be much appreciated please.
I know that are some preliminary guidelines for safe and effective use of repetitive Transcranial Magnetic Stimulation in moderate to severe Traumatic Brain Injury but what is your opinion about neuronal reorganization (particularly language) in severe non-focal brain lesions? The current rationale for TMS use in stroke patients doesn´t quite fit a “TBI brain”. Besides the immediate risk of seizure could also exist some risk of interfering with (good) neuroplasticity specifically in language?
Thank you in advance!
I have been working on a TBI mouse model and looking at AQP4. The literature provided by abcam shows the western blot data to have a band at 46 kDa and another one at 20kDa that they cannot identify. My blots have a double band at 48 and 46 kDa and a large band at 20 kDa. Does anyone have any experience working with this antibody? Any suggestions or ideas about what these bands represent?
Hi, I was wondering if someone could help me a bit to set up an immunohistochemistry protocol for TAU in a model of Traumatic brain injury (TBI) in rats. I have no experience and would like to know which antibody would work better. Also would you recommend fixation of the brains or not? And what should I take into account for this procedure?
Thank you very much in advance
I am a 3rd year student at University of Brighton, UK. I am writing a research proposal, and am struggling to understand the data analysis side of things. all help VERY gratefully received!! I am proposing a study to understand the efficacy of an occupational therapy vocational rehabilitation compared to a non-OT vocational rehab intervention following traumatic brain injury. Purposively recruited sample with TBI. Non-standardised questionnaire asking return-to-work status questions with mainly yes/no answers (eg, 9 questions including are you currently employed, are you currently on sick leave but still employed, how many sick days in past three months). Age and gender being asked. Also a standardised wellbeing score questionnaire (WHO-5). The null hypotheses are 1. The occupational therapy vocational rehabilitation intervention is no more effective than the non-occupational therapy intervention on return-to-work status. OR
2. There is no significant difference in return-to-work status and WHO-5 wellbeing score between occupational therapy vocational rehabilitation and non-occupational therapy vocational rehabilitation subjects.
From my (very basic and little) understanding, I should avoid inferential because that should not be used with purposive sampling (??), but that is about as far as my knowledge goes. We have had very few lectures this year (obvious reasons!), and any help would be grateful received!
I am a mechanical engineer studying brain injury mechanisms. There is enough evidence in literature that thoracic pressure surge due to impact of blast wave in the abdomen or lungs results in brain trauma as a compression wave is transmitted to the brain. I want to know is there is a possibility of brain trauma due to thoracic pressure surge due to non-ballistic injuries in the thorax for e.g. sports injuries or accidents?
I know that are some preliminary Guidelines for safe and effective use of repetitive Transcranial Magnetic Stimulation in moderate to severe Traumatic Brain Injury but what is your opinion about neuronal reorganization in severe non-focal brain lesions? The current rationale for TMS use in stroke patient’s doesn´t quite fit a TBI brain. Besides the immediate risk of seizure could also exist some risk of interfering with (good) neuroplasticity?
I can't figure out why there is not yet an established program looking at the use of ipads to enhance the recovery and community engagement among survivors of TBI. It should be relatively easy to improve quality of life measures and provide greater access to technology tools than before.
I guess there could be difficulties of taking people at vary degrees of technical proficiency, and getting them to use products and platforms to enhance communication in a distributed environment. It would seem to be an interesting idea.
Perhaps improving quality of life measures is too squishy of a goal.
I'm looking to obtain a dataset of brain scans that include only Traumatic Brain Injuries and normal brains. What sites/resources are available for these?
Note: I've checked a few already but seems that TBI scans are very limited
We are currently working on a systematic review and meta-analysis on a new medication for traumatic brain injury. I'm about to include in vivo studies of this drug into the search and analysis. What is the best outcome in these in vivo studies to measure improvement of traumatic brain injury?
For example human have Glasgow Coma Scale, but what is best option for animal models, (except Veterinary Coma Scale) that can be meta-analysed too.
In a level one unit of Complex Neurorehab as an In-patient.
I'm doing an experiment that triggers Traumatic brain injury with a weight-drop method on a mouse. I'm finding the best way to measure microglial activation by Iba-1 Immunohistochemistry on the damaged brain tissue.(Cortex, Hippocampus)
The method I tried was to set the ROI, 1) Intensity of the whole area within ROI, 2) Find the area size (%) occupied by Microglia in ROI, and get the Arbitrary unit multiplied by two values.
(Ref: Berrrrpohl, D., You, Z., Lo, EH, Kim, H.-H., & Whalen, MJ (2007) .TNF Alpha and Fas Mediate Tissue Damage and Functional Outcome after Traumatic Brain Injury in Mice. Journal of Cerebral Blood Flow & Metabolism, 27 (11), 1806-1818.doi: 10.1038 / sj.jcbfm.9600487)
Do I need to use better method to quantify the microglial activation? I also have heard about Scholl analysis, but I wonder if it can be applied to fluorescence images other than DAB stain. I look forward to answers from experienced people.
Platelet transfusion? Desmopressin? rFVIIa? TXA?
Always more frequently in our hospital we have to treat traumatic brain injury in patients receiving antiplatelet medication.
I know there are no unanimously recommended guidelines.
A recent update of european research group on bleeding care in trauma (Spahn et al. Critical Care 2013; 17: R76 -http://ccforum.com/content/17/2/R76 ) recommended:
- to administer platelets in patient with substantial bleeding or intracranial hemorrhage who have been treated with antiplatelet agents (GRADE 2C).
- to administer desmopressin (0,3 mcg/kg) in patients treated with platelet-inhibiting drugs (GRADE 2C).
- to treat with platelet concentrations patient with continued microvascolar bleeding, if platelet dysfunction is documented (GRADE 2C).
Waiting for PATCH study (de Gans et al. BMC Neurology 2010, 10:19 -
http://www.biomedcentral.com/1471-2377/10/19 ), what is your experience about this clinical context? Have you ever used rFVIIa?
Do you measure platelet function in patients treated or suspected of being treated with antiplatelet agents?
The question is as follows. Can Visual Evoked Potentials (VEPs) be used to determine, or at least to get some idea as to which parts of the brain were damaged in a Traumatic Brain Injury (TBI)?
One of my sources said that one structure that could potentially have been damaged in a case where later some changes in VEPs were found to be present, was the limbic-reticular system. That is suggesting that changes seen in VEPs can be traced to specific parts of the brain. It would be great if somebody were able to confirm this and link some reliable sources!
I know there's a lot of information on using PEVs to diagnose and evaluate optic neuritis, glaucoma, and a number of other diseases, mostly ophthalmological. I am only seeking info regarding traumatic brain injury, and I would be so grateful to anyone who'd be able to share anything on that subject.
Thanks in advance!
When treating patients with abnormal tone, I often find recurrent inhibition using a range of sensory modalities from cooling to electrical stimulation at low levels is very effective in some patients. Others respond best to reciprocal activity. Clearly, spasticity results from an inbalance of inhibitory and excitatory activity, but can we deduct or identify which? If so, does that have a direct influence on central or peripheral management of tone? While Botox and other end organ interventions work, I am looking for ways to alter the central activity related to the abnormal tone.
I would like to investigate which specific cognitive or emotional factors influence the quality of life of TBI patients. I am using a subjective checklist to assess symptom severity of cognitive and emotional sympotms and would like to see, which specific items could predict/correlate with QOL most.
To assess overall Quality of life, should I then use a general Quality of life measure such as the Satisfaction with Life scale or a single item scale, or should I use a health related quality of life scale that is specific to TBI (e.g. QOLIBRI) and already includes subscales that also measure satisfaction with cognitive functions?
Any help would be appreciated !
What Research Tells Us About the Birth of New Brain Cells
The above research is considered important as is suggests that there are factors that can stimulate and inhibit the process of adult neurogenesis. It even hints at possible models for treating degenerative diseases, such as Alzheimer's and Parkinson's diseases, and even reversing damage caused by traumatic brain injury.
I am looking for a self-report questionnaire that was specifically developed for the assessment of cognitive complaints experienced by patients that experienced a traumatic brain injury.
Any help is appreciated!
In cases that mild TBI without no abnormalities in conventional MRI or CT, is there any methods evaluating brain damage in the real clinical field, other than diffuse tensor tractography or diffuse tensor imaging?
Does anyone know any CT brain dataset with lesions and patient's behavior? It can be traumatic brain injury, stroke or brain tumor.
I would like to know if anyone is aware of any available online neuroimaging database for patients with traumatic brain injury. I am interested in fMRI,structural MRI, and DTI.
I have been searching online and I found only The BRAINnet Database. So, If you have the knowledge about other databases please let me know.
Thanks in advance.
Do musical children who have acquired tbi adapt and change their brain differently than nonmusical children? How does their musical ability aid in helping them adapt and continue development in educational settings even with the neurological setback?
My lab is seeking at Graduate Research Assistant for a project focused on FEM of traumatic brain injury including biochemical and biomechanical tissue characterization. Please send this link to qualified applicants: http://niml.org/wiki/images/d/d8/FEM_AT.pdf
I've been looking for a suitable model of chronic neuroinflammation, that not involves a Neurodegenerative disease directly. So, I look for LPS model and TBI, wondering which model is better for evaluate chronic microglial activation.
It appears that most caregivers for chronic disabling conditions need similar support - education, medical, rehabilitation [may vary by condition], financial, community integration>
No paper gives me an answer as to why solely using an axonal stretch model to study the effects of TBI is a good idea or why they chose it over studying shearing forces. Can anyone explain what the difference would be on an axonal level?
Like the question says, does anyone know what happened to the Post-Concussive Disorder of Appendix B in DSM-IV, in the DSM-V-revision? Did it end up as the "Major or Mild Neurocognitive Disorder Due to Traumatic Brain injury"? And, does anyone know of good articles that discuss the DSM-IV vs DSM-V diagnoses? Or Discussions of the DSM-V diagnosis and either the WHO, CDC or ACRM consensus definitions of mild traumatic brain injury (MTBI)?
It is already know variations in the circle of willis are associated with intracranial aneurysm formation due to change in the hemodynamic flow. I would like to know what is the likelihood of a patients with UIA, to rupture if he has a variation in the circle of willis, whats is the risk of this aneurysm get rupture.
I know that regeneration happens at PNS to some extend. I'd like to know whether injured (completely transected) axons fuse with the distal part of the axon in the PNS after succesful therapies. Or does the distal part die and disappear and the proximal end of the axon regrow towards the target area?
Could you please attach relevant paper? Thanks in advance.
I am using weight drop method to induce brain injury and do neurological assessment, during and after treatment
It is well known that executive functions are impaired in individuals with anxiety and mood disorders, and that such impairments remain even after successful treatments for such these disorders. Results from some studies suggest that executive function difficulties may even be present before the onset of anxiety and mood disorders and play a role in their development and maintenance. Moreover, complete remission of anxiety and depressive symptoms is not always observed after treatment, and performance on tests that measure executive functions is influenced by one's affective state (stress, fatigue, etc.).
On the other hand, other conditions are typically associated with executive dysfunction and/or can lead to such impairments (e.g. ADHD, autism, traumatic brain injury, and medical conditions such as phenylketonuria (PKU), MS, diabetes, etc.) To complicate matters even more, psychiatric disorders (e.g. anxiety, depression) and general stress, fatigue, etc. are often comorbid to such medical conditions.
That being said, are there measures, specific executive dysfunctions or deficit patterns that can help differentiate executive function difficulties primarily related to psychiatric disorders/affective state from executive function difficulties that are more primarily related to another medical and/or neurological conditions (especially in individuals who present (or may present) with such comorbidity)?
Thank you in advance!
I am planning to run a DTI study on patients with tumors in the anterior and posterior language areas. Do I need to account for a brain mass in the DTI analysis and if yes - how? If possible, please provide me with references.
Thank you so much in advance.
In BrainQ, I've developed a therapeutic device that have shown to increase rehabilitation process in animal model after stroke, SCI, and TBI, where the major phenomena was to regenerate white matter of specific neural networks that lead to re-gaining lost functions. However, one of the main questions is the rate of degeneration of axons after stroke. In our paper we can see that after stroke, 2 weeks later to the stroke, the rat (stroke side) CC is invisible in the MRI/DTI image. I be be grateful to hear your opinion on this mater, which reflect on treatment of people after stroke.
I am trying to finalise my three papers on 'The Physics of Neurological Shock-Waves in the Human Brain due to Improvised Explosive Devices (IEDs)' prior to hopefully publishing them, but I still have a few questions.
Has anyone been able to experimentally measure the energy (and the possible temperatures) within the brain (or a surrogate skull) following a shock-tube blast?
If so, how does the build-up and decay of this energy behave? Do you witness it to behave like a Dirac-delta spike that rapidly peaks and then falls off equally so? Or is it a more gentle transfer that could be modeled by a gradually diffusing sine curve, for example?
Does the severity of the transfer of energy matter in the above two respects, and what fraction of the initial kinetic energy of the incident shock is transferred in the first place?
Any answers to these questions will be much appreciated.
Thank you in advance,
Any one have a validated instrument to measure caregiver burden in TBI (other than caregiver strain index) ?
I am interested in the segmentation of the corpus callosum (CC) into its 5 regions: genu, body, isthmus and splenium. I was wondering, based on the Mouse Brain Atlas (Paxinos & Franklin), what coordinates would you use to separate these regions for coronal sections. I found one paper by Steelman et al. (2012) that gives the coordinates for each region (i.e. 1.34 to 1.44 from bregma for the genu etc.). However, most other papers I found either looked at the human brain, or just briefly mentioned they looked at the genu or splenium, without giving any other details.
Chronic traumatic encephalopathy, CTE, Concussion, Traumatic brain injury, TBI
I would like to do some research on impaired self-awareness and its related topics (error monitoring ; cognitive anosognosia ; self-regulatory processes ; ...). However, litterature about this topic seems mostly related to TBI patients and is lacking in stroke patients (even if evidence -as in USN and anosognosia for hemiplegia - seems to suggest impaired self-awareness in some stroke patients). Does anyone have any clue about such a lack in terms of cognitive processes or cerebral activation ? Thank you.
Traumatic brain injury (TBI) is caused by rapid deformation of the brain, resulting in a cascade of pathological events and ultimately neurodegeneration.
Most of papers and review articles, that I have come across, only talks about abnormally elevated level of lactate in moderate or severe TBI. I could not find any such report in case of mild TBI.
i) Could someone please provide me some reference/s where elevated level of lactate has been reported in case of mild TBI?
ii) We know that neurophysiological and neurological dysfunction resolves with in few days/weeks in most of patients. However, a significant portion of patients with mild TBI (~15%) report persistent cognitive dysfunction weeks, months and years post injury. Could some TBI expert be kind enough to share his/her insight into metabolic imbalance expected in those patients with poor recovery?
Mid aged man presents with 1.5m steel rod penetrating through the skull up to the genitals and beyond attracting all major specialities in one surgical table~ Neuro-Stomatology- ENT-Thoracic-Cardio-General-Uro-Ortho-
We are intending to study the effect of TBI on BF neurons. I did some literature search and found both FPI and CCI model have been used for this purpose. Between these two models, which one will be more appropriate to study the BF?
What we know:
1. Decompressive cranionectomy is used to treat malignant brain swelling from TBI or mass infarction but several studies have come up with non-uniform results
I am dealing with an elderly patient who lived independently then suffered a "mild" cerebral event. She appeared to have fully recovered when she sustained major head trauma. At this point, I'm trying to figure out if she would have ended up in assisted living anyway owing to the natural progression of her condition or whether it was likely that she could have maintained independence absent the head trauma. I need to reach out to a qualified clinician, but don't know if I should be searching for a neurologist or a neuropsychologist.
One of the risk factors when using Transcranial Magnetic Stimulation is a history of severe head trauma, and it is even included by Rossi et al (2009) in their proposed screening questionnaire (A Consensus Statement from the International Workshop on “Present and Future of TMS: Safety and Ethical Guidelines”, Siena, March 7–9, 2008). However, there are many studies examining mTBIs using TMS, how can this be the case? Is it because single pulse TMS is used, as opposed to repetitive TMS?
Could someone please help me understand the difference between neuroendocrine dysfunction and Post-traumatic hypopituitarism (PTHP)?
We're inducing repeated traumatic brain injuries in a closed-skull mouse model.
We chose isoflurane as the anesthetic because it doesn't have the neuro effects that injectables such as ketamine/xylazine do, and because it allows for quick recovery in order to be able to observe signs of TBI immediately.
It appears that after being anesthetized and impacted once (great recovery the first time), the mouse died during prep for the second impact. Isoflurane dosage was roughly the same as the first, successful impact, but the mouse died ~2-3 min after removal from gas chamber, at which point it was slightly under-anesthetized.
Is there a way to reduce the anesthesia dose while keeping the animal unconscious for the procedure? What differences in response to isoflurane would you expect in C57BL/6 mice? (the mouse above was BALB/c), and how would the mouse's age affect that prediction?
One aspect we lag behind in management is the timely rehabilitation in patients with TBI. Can anyone advise on the rational approach for the same in the resource restrained setup ?????
I have been practicing placing back the craniotomy flap on the open dura and the temporalis flap and never had a problem in the immediate post operative period and or the late period. I am aware of the various options and do practice the placement of the free flap in the parietes of the abdomen. On surveying the literature I couldnt find any study suggesting the possibility of a sinking flap. I wonder if I missed on any such study. I would like help on this issue.
Have you ever mounted a camera (e.g. GoPro) to your helmet and wondered if it was safe to do so?
The effects of helmet-mounted cameras on safety performance were recently investigated by TRL (see links), concluding that such cameras were not as influential on safety as first feared. TRL identified, however, that their results were valid only for specific impact configurations; and that variables of impact mechanism, helmet/camera design and camera mounting configuration could all significantly affect these conclusions.
Currently there are no safety standards concerning the standardised type-approval of helmet-mounted accessories. With the recent explosion in the popularity of helmet-mounted cameras, however, should this be something that changes to ensure wearer safety?
One of the frequent side effects of TBI is depression.
Also known is that the side effects of medication ( SSRIs et al ) can be magnified in such patients, even in small doses.
Subsequent to the development of Prozac, all work on possible alternative supplements to improve serotonin ceased. It was argued, that L-Tryptophan and/or 5HTP did not pass the blood-brain-barrier.
Subsequently, I think that this has been shown not to be the case, and that both can affect an increase in Serotonin levels in the brain.
Are readers aware of any such research to support this view or would like to comment on this contention.
He underwent suboccipital decompression and is improving. Anyone else seen or dealt with such a case?
Does anyone have an idea or that overuse of the neck can cause cerebral infarction resulted from thrombus in the internal carotid artery?
A 61-year-old male was brought to the emergency department with complaints of left side paralysis and speech disturbance. The symptoms supposedly appeared while he was sleeping. Apparently, the patient could not move his left hand and leg. He was alert and his blood pressure was 120/60 mmHg. He has no history of hypertension, diabetes, or hyperlipidemia. He does not consume alcohol or smoke. According to his wife, he complained of right side neck pain in the preceding day after he played Kendo _ Japanese martial art. There were no apparent bruises or wounds in his right neck.
USG revealed the thrombus at the trunk of right internal carotid artery. CT revealed no bleeding but the high intensity lesion in the right middle cerebral artery, indicating clots in the vessel. MRI showed the high intensity lesion in the right basal ganglia. MRA showed the deficit of the blood flow in the right ICA. Then, he was diagnosed as acute stroke resulting from thrombosis in the ICA. Thinking of the interval of the onset, he was not considered as a candidate of interventional radiology followed by iv t-PA treatment. Then, conservative treatment by edaravone and antithrombin agent were initiated.
In this case, I wonder if there are some relationships between sports and cerebral infarction. I am interested in the involvement of external force or overuse of neck as the cause of his illness.
Does anyone have experience in neuromonitoring? What indications for brain tissue oxygenation monitoring in patients with severe traumatic brain injury? For all patients severe TBI or who have some risk factor?
There are many studies that have found evidence of chronic hypopituitarism in patients at least 1 year after injury. Routine screening for chronic hypopituitarism after brain injury shows promise for appropriately directing diagnostic and therapeutic decisions that otherwise may remain unconsidered and for markedly
facilitating recovery and rehabilitation.
We recently concluded a study on the prevalence and characteristics of maxillofacial injuries in patients with mTBi, and analysed the possible influence of maxillofacial (MF) trauma over specific cognitive deficits post trauma (namely executive function, memory and attention). We also looked out for WM tracts that were affected both in the acute and follow up phase [controlling for both the presence of maxfac injuries and as well as the CT imaging findings (intracranial lesion vs. none)]. The results were quite interesting and seem to challenge the conventional understanding and management of patients with mTBI.
We found that patients with maxillofacial injuries without intracranial lesion doing significantly worse over time in the domains of executive function and memory. Miscrostructurally, these patients seem to have poorer WM integrity especially involving the projection and association fibers (mainly corona radiata, cingulum, superior longitudinal fasiculus, optic radiation and genu of the corpus callosum).
Would appreciate your thoughts on the biophysics and biomechanics of maxillofacial trauma in mTBI and how that could explain the findings.
Research shows (e.g. Shalev et al., 1998; Orr et al., 2008) that people diagnosed with posttraumatic stress disorder (PTSD) had significanly higher heart rates in the ER and at 1 week (but not 1 and 4 months) post-trauma than those who were resilient to PTSD. A high percentage of people with mild traumatic brain injury (mTBI) also develop PTSD. Do those people brought into the ER for head trauma who later develop PTSD show elevated heart rates compared with the heart rate of mTBI patients who do not develop PTSD?
My current data on neuropsychological performance in patients with mTBI across two time points (admission vs follow up) indicate that although the patients with the cortical injury do significantly worse in almost all domains of neurocognitve assessment during the acute phase, these patients, however, outperform the patients with "plausible" axonal injury (based on the DTI data) in the follow up phase (6 months post trauma)? What do you think is happening here?
Can someone suggest me any research/study on using the Kaufman Brief Intelligence Test to assess Trauma Brian Injury (TBI)? And particularly, is the unusual large discrepancy between verbal and non-verbal scores in K-BIT indicative of TBI? or does it just raised concerns about general cognitive abilities that need further assessment? Thanks
Traumatic brain injury, even in its mildest form, is known to result in degenerative processes including demyelination and dysmyelination of the axons over time. The shearing and tearing of the axons (primary injury) due to the acceleration and deceleration force of high velocity impact would also normally trigger off the secondary injury cascades. This includes the synaptic deregulation, cell death and axonal degeneration.
But how quickly does these processes start (especially the demyelination of the axons) in patients with mild TBI? I am of the opinion that it will take at least a few days or weeks before such degenerative process starts. What are your thoughts?
I have a 15 year old patient who had a concussion 2 years ago. Her parents report that she is unable to recall past events, As an illustration, they said in the past summer she spent a week at the shore with her friends. With coaching she can remember the event but can recall no details of the vacation. They claim she never had this problem before the concussion.