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Traumatic Brain Injury - Science topic

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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
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There is a substantial literature on this. Search an academic data base (Psych, Educational, Medical journals) for TBI and Applied Behavior Analysis (ABA) or TBI and Cognitive-behavioral interventions.
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Hi everyone,
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.
Thank you
&
Regards
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Claudio Pedrazzi
Thank you professor, i will look for it.
regards
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Hi,
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...
thanks
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Maybe ELISA would be more suitable? Section staining is good for seeing the location of the signal and is much worse for estimating the strength of the signal, especially if the reduction is mild. Western would be also suitable, especially if you have optimized the protocol.
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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.
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Yes but you have to eliminate the duplicates and make sure you can identify studies from the same centres as they might be reporting the same data.
Worth mentioning that making a single publication (your cohort study together with a systematic review & meta-analysis. Bearing in mind that SRMA is a distinct endeavor in itself, with rationale, methods, results, discussions (with limitations) and conclusions not just pooling of data
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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!
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Here are some references for TMS in stroke patients with language deficits:
Naeser, M. A., Martin, P. I., Nicholas, M., Baker, E. H., Seekins, H., Kobayashi, M., Theoret, H., Fregni, F., Maria-Tormos, J., Kurland, J., Doron, K. W., & Pascual-Leone, A. (2005). Improved picture naming in chronic aphasia after TMS to part of right Broca's area: an open-protocol study. Brain and language, 93(1), 95–105.
Naeser, M. A., Martin, P. I., Nicholas, M., Baker, E. H., Seekins, H., Helm-Estabrooks, N., Cayer-Meade, C., Kobayashi, M., Theoret, H., Fregni, F., Tormos, J. M., Kurland, J., Doron, K. W., & Pascual-Leone, A. (2005). Improved naming after TMS treatments in a chronic, global aphasia patient--case report. Neurocase, 11(3), 182–193.
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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?
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I have been looking into this, as well. I have seen bands at ~90kDa, at ~50kDa, and at ~20kDa. Primary literature points to the ~90kDa band as likely some SDS-insoluble oligomer. But, I can't seem to find anything for the 20kDa band. Have you found anything yet?
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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
Kind regards
Rodrigo
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William Kwan thank you very much!
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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!
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Many thanks, Peter, that's a great help!
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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?
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Following.
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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? 
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Good Answer Vladimir A. Kulchitsky
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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.
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I think this is a terrific idea for a number of reasons. Many TBI patients have become socially isolated due to their embarrassment about their deficits or even due to disinhibited behaviors that have alienated family and friends. Engaging with others on a online platform can provide an intermediate step toward reconnecting with people and the community in general. Of course, some patients with cognitive deficits may need some assistance with the technology itself and the hope would be that a TBI clinic case manager or other helpful person could fulfill this function. Eventually, online measures of life satisfaction could be introduced to monitor and document positive effects of patients' use of this technology.
Incidentally,the recent second edition of my Manual of Inpatient Psychiatry (Cambridge U Press) has an entire chapter on TBI that can provide background material of relevance to this question.
Michael Casher MD
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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
Thank you!
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Please mention here...if you have found out any datasets for TBI CT scans
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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.
Thank you
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It is not my topic by my approach here would be
i) identify the outcomes that have been used in studies you have already identified in preliminary scoping searches
ii) engage with topic experts about the most important outcomes to use although I think that it is likely to be hard to identify a clear primary outcome in such animal models unless mortality is relevant (maybe it is?).
iii) if there are no (or few) studies then the question is moot - you've not got anything to meta-analyse any way!
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In a level one unit of  Complex Neurorehab as an In-patient.
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...how long...years??
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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.
Thanks.
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Markley Silva Oliveira-Junior Thanks for your comment. I have CD-68 antibody to detect macrophage in brain tissue. And there is specific brain region to analyze. (Cortex and Hippocampus CA3 region) I have not thought about using antibody CD-45 together with CD-11b and CD-68. However, I need to apply the technique you introduced to me. Thank you for your kind feedback.
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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?
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Desmopressin has no significant hemostatic effect in connection with
trauma and massive bleeding but can be useful if there is a simultaneous
platelet function defect or in certain forms of VWD. Desmopressin is often
combined with tranexamic acid.
For dosage and special considerations for treatment
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Hello!
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!
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Tamer Roushdy, thank you very much for replying! I understand that I would probably have had better luck if I tried searching other types of EPs instead of just focusing on VEPs, although that's my exact current search task, and I am not the one choosing the objectives. Nonetheless, thank you for your insight!
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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.
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Hi,
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 !
Thanks!
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You can check out our contribution to satisfaction with life:
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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.
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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!
Thanks!
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NINDS Common Data Elements is usually a good place to start your search (https://www.commondataelements.ninds.nih.gov/TBI.aspx#tab=Data_Standards). Under the Patient-Reported Outcomes section you would find several relevant measures. I'd probably opt for the TBI-QOL - it also assesses several other domains apart from cognition.
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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?
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Have you tried with DWI sequence.
If the damage is in Gray matter, then you can go for FDG-PET.
Thanks
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Looking for resources, comments, or general explanations! Thank you in advance.
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With aphasias the language of the thoughts of the patients is the same as the language they articulate. This is seen when they are made to write down their thoughts, provided of course their writing ability is not affected due to paralysis of their writing arm. thanks.
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Dear all,
Does anyone know any CT brain dataset with lesions and patient's behavior? It can be traumatic brain injury, stroke or brain tumor.
Thank you,
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Po-Yu Kao : You can get in touch with the Director of the Radiology department of your University and present your request. But as a practicing neurologist I do not see how doing this type of study on CT scans will help us. The CT scan is of very limited use to us now. Even MRI, except for fMRI, is becoming less valuable from research point of view. Brain PET, SPECT scans using specific radioisotopes for specific neurotransmitters, receptors, transporters is what translational research in neuroimaging has become in neurology. There are now medical centers where only MRI is being used for clinical neurology, even for stroke, whether ischemic or hemorrhagic. My intention is not to discourage you, but just to tell you what we neurologists are interested in regarding brain imaging. thanks.
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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.
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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?
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Caitlin,
Probably so - I would interpret this question in the context of cognitive reserve. The following papers focus on cognitive reserve in adults but it can theoretically be applied to children as well.
Stern, Y. (2002). What is cognitive reserve? Theory and research application of the reserve concept. Journal of the International Neuropsychological Society, 8(3), 448-460.
Bigler, E. D., & Stern, Y. (2015). Traumatic brain injury and reserve. In Handbook of clinical neurology (Vol. 128, pp. 691-710). Elsevier.
I hope this helps!
-Ryan
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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
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Hello Prof Bryn
Projects seems nice and novel. I am interested in MS.
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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.
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Greetings. TBI is certainly a very good way to study chronic neuroinflammation. However, TBI is a spectrum and you need to choose which part of the spectrum is suitable for your studies. mTBI does have inflammation but the degree of inflammation may be too mild for the sensitivity of your studies. perhaps CTE will suit your studies the best and it has tremendous practical, social especially, impact. thanks.
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It appears that most caregivers for chronic disabling conditions need similar support - education, medical, rehabilitation [may vary by condition], financial, community integration>
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Любое долгое хроническое тяжелое заболевание пациента создает вокруг ауру, куда попадают как родственники, так и сиделки. Проще справляться и понимать, что происходит, если обладаешь не только знаниями о заболевании, но и психологической поддержкой. По-моему, идея замечательная!!! Только, наверно, нужно учитывать психологическую дистанцию между пациентом и ухаживающим, и смотреть, что на нее влияет, как сделать ее комфортной и не приводящей к выгоранию.
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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?
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i think the different areas of the brain undergo different kinds of injuries in TBI. the brain stem twists, the frontal and occipital lobes, especially the poles, goes through compression and the basal forebrain goes through shear. this is a wonderful question. the next question is how can we find evidence for these different types of axonal injuries. mustafa.
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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)?
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Post-concussive syndrome is a controversial and (scientifically) poorly defined entity. PCS is used by clinicians to mean all sorts of different things. The DSM-IV criteria were for research use, not clinical use, and were never generally accepted. DSM-V therefore dropped the diagnostic construct; persistent symptoms after a concussion should lead to  consideration of DSM-V neurocognitive impairment, somatic symptom disorder, or non-psychiatric causes. Given current knowledge, the special case of comorbid PTSD and TBI (in my opinion) muddies the waters rather than illuminating common mechanisms. 
From the standpoint of a clinician (I'm a neurologist), the majority of patients seen in, for example, a "concussion clinic" will have a minimal or mild TBI by HISS (Stein) criteria. There is ample evidence that - in marked contrast to moderate or severe TBI - symptoms persisting beyond 90 days are mis-attributed or are psychogenic. The high frequency of pseudo-neurologic presentations and the importance of accurate subjective report in otherwise "objective" testing (for example, of vergence, which is also affected by fatigue, congenital muscle imbalance, drug exposure, etc) needs to be kept in mind in these often complex cases. 
The best available introduction to the science here remains:
{McCrea, 2007, Mild Traumatic Brain Injury and Postconcussion Syndrome: The New Evidence Base for DIagnosis and Treatment}
And of course Iverson's work including application of the concept of "Biopsychosocial" impacts on presentation.
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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. 
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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.
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Thank you very much dear Anup.
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I am using weight drop method to induce brain injury and do neurological assessment, during and after treatment
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I have found the rotarod with 1 mm bars the most sensitive for motor outcome. See Hamm et al, J Neurotrauma 1994, 11:187.
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Particularly in set up where the resources are limited
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In a resource limiting setting:
  • Persistent GCS <15
  • Suspicion of depressed skull fracture
  • Focal neurological deficit/ repeated seizures
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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!
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"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"
I do not understand why any difference is to be expected.   Symptoms like pain, hallucinations,  poor memory, etc.,  are basically similar whatever their supposed cause.
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Dear Colleagues,
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.
Monika
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What type of brain tumors do your patients have? Have the patients had biopsies? DTI would be affected by the type of tumor, whether it is infiltrating or well-circumscribed. If my understanding is correct, tumors infiltrating the white matter have a larger impact on DTI metrics.
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What are the reasons that make healing of meningitis and encephalitis difficult 
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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.
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Dear Emmanuelle
BrainQ is a company that was created to resolve neurological deficits by means of enhancing natural rehabilitation processes of neural networks. It started where my son, Lear, was born with a rare genetic disorder that affect the CNS. In the process of understanding what is his exact "problem" I've discovered that many other nervous syndromes and impairments share similar characteristics to my son syndrome. Then I've developed a conceptual model for intensify rehabilitation processes in the brain (and spinal cord). Once pre-clinical trials have shown first signs that the concept is feasible, BrainQ (Brain cue to cure) was formed. The principle of the treatment is a very low intensity and frequency electromagnetic stimulation which sync to the way neural networks work, and by that, promote their re-growth, and by that, increase the chances and extent of rehabilitation after impairment. Since BrainQ have showed very impressive pre-clinical results (TBI, Stroke, SCI), BrainQ, as a compaby was formed. Right now we are conducting a clinical trial that is focused on spinal cord injury (were he people are about 6 months and longer after the injury, which brought me to ask how "post acute" .vs. "chronic" are they). We are seeking collaboration with researchers who are interested in clinical trials. We have published two papers about Stroke and SCI, and now in the process of publishing our paper about TBI.
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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,
Stephen Mason
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Thank you Michael.  Others also suggested to me that torque and head/brain rotation/acceleration, for example, are indeed important factors in head injury - particularly blunt impact phenomena sustained in accidents and sports injuries - but I decided not to go as far as that for various reasons (not least because of the sheer volume of my existing work).  I am hoping to eventually publish, but it all depends on the peer review process along with any corrections that are required - some of which I have already noticed dotted here and there in my papers.  I am not sure if I can say anything more about my work at this stage but, by all means, do look out for it. Regards.  Stephen.
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anyone research can answers
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Hi Norly,
All the terms you referred to in your question are multiple-word terms, i.e., compound words. "Neuro-" in Greek stands for neuron; "development" refers to the process of natural progression from a previous to a later stage; "science" is a systematically organised knowledge on a particular subject. Finally, "cognition, a Latin word, embraces the quality of knowing (perceiving, recognizing, judging, reasoning, imagining, etc.) 
Hope this helps. Kind regards, Tatyana
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Is there some form of imaging that can be used for remote anoxic injuries (neonatal-years later)? Perhaps something that shows reorganization?
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An HMPAO perfusion SPECT scan is the best method.
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Any one have a validated instrument to measure caregiver burden in TBI (other than caregiver strain index) ?
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Rate in percentage
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You can contact our sports med person
john.palmer@usma.edu he should be able to provide some information to you. Let him know I passed along his name
Thanks
Lynn
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Hello,
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.
Thank you.
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I agree with Shafagat Mahmudova good references. thanks
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Chronic traumatic encephalopathy, CTE, Concussion, Traumatic brain injury, TBI
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"I do not think there is any connection between concussion and CTE"...
...or between concussion and other forms of brain injury.
There is a photo in today's Times of Ryan Mason lying on the ground after a clash of heads at Stamford Bridge that left him with a fractured skull.   He is on his side holding his right hand over the point of impact, so it is very unlikely he was unconscious or concussed.
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I am looking for someone who works on Depersonalization-derealization disorder and TBI ?
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My guess is that depersonalization is connected with minor head injury, not traumatic brain injury, so you may be better off looking for those working in post-concussion syndrome. 
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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. 
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Hi Samuel,
I think there are several possible explanations:
1. Because self-awareness is usually linked to prefrontal areas of the brain researchers choose this clinical population since brain pathology in TBI most often includes injuries of frontal lobes (hemorrhages, bruises, contusions, shearing etc.). On the other hand, lesions in stroke are most often located in the teritory of MCA. Strokes in prefrontal areas are rare, although hemorrhage from ACoA aneurysm leads to similar (dysexecutive) symptoms.
2. Of course it doesn't mean that unawareness cannot be seen in patients after MCA stroke. In fact most (or even all in acute phase) patients with neglect have limited awareness, just as you mentioned in your question. However, it is extremely difficult to design a research on patients with severe aphasia who most certainly have deficits in self-awareness as well. In case of UNS, in turn, researchers usually focus on the most prominent disorders which is space perception difficulties (although improvement of awareness is ALWAYS one of the goals in rehabilitation).
3. Age matters. However it sounds. It's much more likely that a 30-year-old working man has no history of pre-injury cognitive (and meta-cognitive) problems than a 80-year-old (approximate mean age of stroke patients) retired individual with stroke.
4. Some anosognosic symptoms after stroke withdraw quite early - during first hours or days. Take Anton's syndrome for example. I have never seen it lasting for more than a week or two.
Hope it helps a bit,
Marcin
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Traumatic brain injury (TBI) is caused by rapid deformation of the brain, resulting in a cascade of pathological events and ultimately neurodegeneration.
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Antonio is right - for the outer layers! It is a good starting point, but be aware that TBI happens all over the brain and thus you have to take a complex model of brain anatomy into consideration: Already thin sheets of meninges have a huge effect on the mechanics, fiber bundles behave non-homogenously, ventricles are not just water filled holes, blood vessels extend from a visible size down to capillaries with an average distance below 100µm...  So, be aware of the limitations of a mechanical gel-model!
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84 year old head trauma patient (with brief LOC).  
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 Thank you for pointing out RBANS, your response was very helpful.
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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?
Regards,
Dushyant
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Hello Dushyant Kumar
please check the resources and one of the pdf is discussed in detail about TBI
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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-
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Did the patient arrive alive to the trauma bay? If yes, I would apply the ATLS premise that you treat first what would kill faster.
it doesn't look like his major vessels were affected. He will likely have neurological sequela since it looks like his frontal lobe was damaged.
Please let us know how it went.
Best regards,
Alice Gallo
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Hello everyone. 
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? 
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Dear Nanthini Jayabalan,
Both models are adequate to study TBI as are both well described in rats and other animals. I think I would choose the CCI model for this purpose (BF) because it can produce a more localized injury. Please take a time to read this paper, it may be of value to you:
Best regards,
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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 
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Depends on extent of edema and shift. Anterior temporal lobectomy or decompressive craniectomy appears to be the last resort.
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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.
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You need an Occupational therapist to assess the person's capacity to perform Activities of daily living and discuss it with the neurologist. There are tests they can do in relation to cognitive capacities that assess the ability to perform practical activities that go with living alone. They can arrange other services that might be needed at the home, such as showering, meals and tnrasport.  They will then discuss these with the Neurologist. 
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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?
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Thomas
Basically, you should not use TMS in patients with history of brain injury
in your research lab if you cannot provide qualified medical assistance -
take a look at the table 7 from Rossi et al.'s guidelines. Many rTMS and
tDCS studies have been conducted even on severe TBI but they are usually
carried out in hospital settings. That is the first condition. The second
is informed consent from your patient and ethical committee agreement. The
aim of your research is a crucial issue. If the results may help find a
new treatment for individuals with brain injury the choice of a clinical
population is justified. If it is just for fun, well, you can always ask
your healthy colleagues to participate in your experiment... Anyway, you
need to assume that there is ALWAYS some risk.
Good luck
Marcin
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Hello,
Could someone please help me understand the difference between neuroendocrine dysfunction and Post-traumatic hypopituitarism (PTHP)?
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Posttraumatic Hypopituitarism
Vatroslav Čerina 1, Krešimir Rotim 1, Darko Stipić 1, Milan Vrkljan 1, Hrvoje Ivan Pećina 1, Damir Kruljac 1, Jelena Marinković 1
J Neurol Surg A Cent Eur Neurosurg 2015; 76 - A102
 
Neuroendocrine Disturbances after Brain Damage: An
Important and Often Undiagnosed Disorder
Fatih Tanriverdi and Fahrettin Kelestimur *
J. Clin. Med. 2015, 4, 847-857; doi:10.3390/jcm4050847
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Christiane Albert-Weißenberger
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Traumatic brain injury in humans can be divided into
  1. Specific damage to brain tissue, as shows up on scans, analogous to brain injury after strokes.
  2. Generalized brain damage as can be picked up by tissue products in the blood stream, yet to be shown to be of clinical relevance.
  3. Specific neurological syndromes, as seen in boxers, eg EDH, CTE, etc.
    Many animal models have tried to mimic concussion, which I think is irrelevant as it is probably due to temporary dysfunction of the vestibular reflex system originating in the inner ear, and nothing to do with the brain. 
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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?
Thanks!
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How did you judge that the mouse was under-anesthetized? Under-anesthetized means  that the mouse seemed light in anesthesia?
Dying of anesthesia might be a "sign" of the first TBI; sounds stupid, but we are very concerned to anesthetize TBI (clinically) and therefore I would not exclude this option.
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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 ?????
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A patient of mine who had TBI years ago from an MVA , with coma , subsequent motor and cognitive deficits and disfigurement, had spent a very long time in various excellent inpatient and outpatient  neuro-rehabilitation programs.
He shared with me a book, written by a U of Penn English Professor's husband. A true story about his experience and hers going thru recovery with top inpatient and outpatient facilities. The Book Title is Where is the Mango Princess.  don't  be dissuaded by the title.
Where Is the Mango Princess?: A Journey Back From Brain Injury Kindle Edition
by Cathy Crimmins (Author)
4.8 out of 5 stars 103 customer reviews
"5.0 out of 5 stars What an Amazing Book !!, October 15, 2000
By
BeachReader
This review is from: Where Is the Mango Princess? (Hardcover)
Cathy Crimmins has taught us all a lesson in this book.....that life isn't always as we had thought it would be and that we must be proactive in order to change it.
When her husband, Alan, a successful bank attorney in Philadelphia, suffers a Traumatic Brain Injury (TBI) in an accident, his life and his family's lives change forever. Crimmins takes us through the extensive rehab process which she handles with both tears and laughter. As a reader, I found myself experiencing feelings of anger, hope, sadness, and joy at the smallest improvement in her husband's condition and at the smallest victory over the system.
I could not believe how much I learned from this book. It should be "must reading" for everyone who works with brain-injured patients and also for all of those insurance company "voices on the phone" who make life and death decisions based on very little information, and with very little empathy. I learned about something called "perseveration" which is when a brain-injured person repeats an action or phrase over and over and over again. I also learned that with brain injuries such as this, inhibitions disappear, which means that socially inappropriate behaviors are often displayed. Crimmins also made the reader understand why these patients and their families become so frustrated. I could fill pages with what I learned.......
I read this book in one day and a friend who was visiting me read it the next. I then passed it on to my daughter who also read it in one day and then recommended it to her neurobiology professor who thought it was outstanding. If I had the power to make this book a bestseller, I would!"
This book I now require residents in GME training to read and perhaps it should be read at Medical Schools and by faculty.  Although written for the lay person, it provides insight and empathy for those who experience TBI and various recovery phases. Realistic STG and LTG enable coping strategies to kick in when despite remarkable or miraculous improvement the subtle cognitive and personality changes may never fully recover and (spoiler alert) preclude to previous employment setting (in this case a high powered Philadelphia law firm)
You will never look at someone with TBI (however minor appearing) the same again- this book can be trans- formative for patient's significant others and to physicians in creating true compassion.
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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.
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There has been a recent study on performing  window technique while replacing bone flap back in suspected cases of malignant traumatic cerebral odema....We half the bone flap in middle then replace and fix its corners with the parent bone. 
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Rehabilitation hospital art therapy programmes
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We have experience with music therapy and theatre as a way to improve emotional involvement and then responsiveness.
The following article is part of this experience
Brain Inj. 2012;26(10):1250-6. doi: 10.3109/02699052.2012.667588. Epub 2012 May 22.
Increased behavioural responsiveness with complex stimulation in VS and MCS: preliminary results.
Di Stefano C1, Cortesi A, Masotti S, Simoncini L, Piperno R.
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Using role-playing games to treat traumatic brain injury video and supporting documents and details.
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The backdrop of the whole "role play" therapy techniques is probably JL Moreno's Psychodrama approach - very large literature on various populations. See:
The Philosophy, Theory and Methods of J. L. Moreno: The Man Who Tried to Become God by John Nolte
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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?
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Martin, 
Such industry light mounted helmets are designed for objects hitting the helmet (usually small-medium objects), rather than the helmet hitting a large object (eg a car or a road) at speed. 
These seem like two different mechanisms, but in both mechanisms a quick release mounting seems sensible. 
Patrick
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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.
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It is true that one of the common sequelae of TBI is mood disturbance with up to 50% of TBI patients experiencing depression within the first year of injury.  And yes, the "TBI brain" is more sensitive to side effects of medications, necessitating a slower titration and an attempt to utilize the lowest effective dose.  Nonetheless, SSRIs such as citalopram and sertraline have shown some effectiveness in TBI-related depressions, as have SNRI's.  The use of TCA's and MAOI's may be more problematic, but we do see lower doses of TCA's used for chronic pain in some head injury programs.
It is also important to keep in mind that depression in TBI is related not only to pathophysiologic changes from the shearing forces of injury, but also can have a psychological component related to--among other factors--the loss of the "old self" and the mourning process secondary to the decline in functioning.
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He underwent suboccipital decompression and is improving. Anyone else seen or dealt with such a case?
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It may be a sequel to central downward herniation in some cases of severe TBI. But we have to rule out the findings of traumatic SAH in the initial CT scan of the patient.
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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.
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Hi Nobuhiro
There is one case report published on this (Suzuki et al, 2012). The patient was a 66-year-old male who presented with left hemiplegia after having recieved a frontal thrust (tsuki) during the practice of Kendo. The authors state that the frontal thrust of Kendo can cause cervical artery dissection and stroke, but that's quite rare.
The reference is the following:
Hope this is helpful to you
All the best
Rodrigo
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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?
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GCS < 8
ICP >25 
OBLITERATION OF PEIMESENCEPHALIC CISTERNS IN THE CT SCAN
PATIENT  DECEREBRATE AND DECORTICATE POSTURING
MICRODIALYSIS- LACTATE:PYRUVATE RATIO > 23
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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.
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I have to admit in regard to children with TBI, there is no consensus in regard to routine endocrine referral or follow up in our institution. I think among ptuitary hormonal output, GH has received better attention though. in the just published review by Gardner & his group, it seems that long hormonal were less dramatic in comparison to non0functioning ademonas, but quality of life were moderate to severely affected nevertheless.  doi: 10.1530/EJE-14-0654.
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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.
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Also the energy used in the process of breaking such hard bones is not available to go through to harm the underlying tissue (that's what a safety helmet does or a football helmet, for example - helmet is toast so the tissues underneath are not).  It is also why you have to replace a bike helmet every 3 years or after any accident - the lining materials are no longer useful as an energy trap and the energies of a blow go right through.  But the majority of the brain parenchyma is only loosely associated with the pia mater so it is the blood vessels (which run through the arachnoid and have to deal with entrances and exits through bones) and the white matter tracts (which are ultimately attached through the brain stem to the spinal cord and which run through longer spaces within the brain, connecting grey areas) that are vulnerable to the energies of an acceleration/deceleration injury.  The exception of course is the olfactory bulb and tract which run through bone and get sheared off leaving folks unable to smell in frontal injuries and accel/decel ones all the time.  Have you thought about doing a simple olfactory screen with your patients to document that kind of injury?
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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?
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Hi Gina,
Great to see this direction in your research! The only comment I would make to your query is that injury to the insular cortex and cerebellum often is a consequence to TBI, partially directly through indirect perfusion changes by middle cerebral artery alterations to injury, partially through direct trauma to the lateral skull, and to the cerebellum, from direct trauma, including damage to projecting fibers from the trauma. Those areas are especially affected by chronic irritants, such as hypoxia from obstructive sleep apnea, perhaps operating through alterations in the blood brain barrier caused by OSA. The right insula is badly hit in OSA and heart failure. Momentary changes in the BBB should not be overlooked in acute injury as well. The reason the insula is important is, of course, the significant role that it plays in regulating the baroreflex and heart rate, well documented by Oppenheimer, Henderson, and ourselves. Stroke injury to the right insula is typically followed by myocardial infarctions two weeks later, probably as a consequence of increased sympathetic tone. The cerebellar role is also important for transient changes to heart rate, because of its dampening role in modulating blood pressure through its fastigial nuclei; the incredible sensitivity of the cerebellar Purkinje neurons and the climbing fibers to injury have substantial potential to modify overall sympathetic tone, and thus, heart rate. That area also possesses substantial plasticity, so that recovery is eminently possible. A very complex story, and a very interesting one.
Ron
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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?
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To keep it simple, let's say that neurons exhibit notable plasticity when still viable whereas axons and axon tracts, to much lesser extent when damaged.  Depending on the cortical areas and activities involved, there are vastly different levels of redundancy and neuroplasticity.  Often, cortical neuronal damage may be treated by activating parallel pathways (neural network approach as evidenced by Carrick, recently on a study of 200 soldiers, victims of blast injuries).  And that, dear sir, brings us to pathways....  Axonal damage means that the corridors of communication are disrupted and therefore cannot pass information from one area of the brain to another...depending on function and redundancy, naturally.  Neuroplasticity is compromised more by axonal damage, and the risk of diaschisis is superior in axonal damage due to a domino effect that direct cortical damage, especially in the higher centers, manifests less.  However, if the axonal damage is significant in the more medial and caudal pathways (cord to brainstem/cerebellum, brainstem/cerebellum to mesencephalon, mesencephalon to thalamus) the manifestations will be much more pronounced than in supratentorial axonal lesions.  That make sense, right?  There are more connections from the more primitive areas of the brain when compared to the more recently developed cortical areas.  We can liken this to damage to a tree trunk that has larger implications to the tree's functions than damage to an area of tiny branches and leaves.  Unfortunately, in mTBI, the major damage is to central structures where axonal damage has more pronounced domino-effects that dramatically effect the basal ganglia, with it's consequent motor, cognitive, and limbic manifestations.
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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
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The Kaufman Brief Intelligence Test is part of the brief intelligence tests that are useful in a screening process. Only serves to estimate overall level of intellectual Functioning in conditions similar to those used in the validation, and the test performance may signal the need for a thorough assessment with neuropsychological measures
We can´t interpret the unusual large discrepancy between verbal and non-verbal scores in K-BIT as indicative of TBI, because the test validity do not provide sufficient evidence for diagnosis, and the estimation of these discrepancies in a short test can lead to an increase in estimation error. You can find people without TBI are presenting large discrepancies or people with TBI who has no.
In these cases, I recommend to do a complete neuropsychological assessment, regardless of whether there is discrepancy between verbal and non-verbal scores.
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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?
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Dear Timothy Shea,
The "miserable minority" are those patients with mild traumatic brain injury who continue to experience prolonged cognitive deficits even after months and years, way beyond the average cutoffs (which is about 3-6 months post trauma).
You were absolutely right that one should consider preexisting comorbidities/(maybe even age) factors and as well as neurobehavioral/ neuropsychiatric condition arising from the trauma that could adversely influence the cognitive performance of these patients. Having said that, there are many studies (Ref 1-5) that has proven that even when all these factors are accounted for, and removed from the analysis, these individuals continue to exhibit deficits in their neurocognitive functions. So what then would best explain these manifesting derangements/ impairments ?
One possible explanation may lie in the structural changes. Patients with visible injuries -complicated mild TBI (radiologically visible lesions  i.e hematoma, contusion, edema, etc) and the corresponding functional and cognitive deficits are findings that are widely accepted by scientific community. How about the wider group of mild TBI patients whose radiological findings are usually negative and discharged from the ED without even being seen by neurosurgeons and without any subsequent follow-ups? Does normal CT/ MRI in the acute stage means there isn't any injury to start with with?
Many advances imaging protocols have proven otherwise. Diffusion Tensor Imaging (DTI) studies (reference to which I will give at the end of this reply) for example are able to pick up changes to the microstructure like the axons or the white matter tracts which are usually missed by the CT/ conventional MRI sequences. Could these structural anomalies/injuries then  explain the neurocognitive impairments experienced by the "miserable minority"? I guess the answer would be affirmative (see ref 5-8). With all these new evidences of microstructural abnormalities (even at the earliest hours post trauma), we can no longer reject the patient experiences as purely psychogenic in origin, ensuring we do our due diligence. 
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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.
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Hi Bruce,
I worked in a multidisciplinary concussion clinic for children and adolescents during my residency at John's Hopkins School of Medicine and the Kennedy Krieger Institute. This is a very atypical presentation for concussion. She needs to be referred for a comprehensive neuropsychological evaluation with a clinician familiar with concussion. Subjective reports of anterograde memory impairments following mild TBI can be associated with a number of underlying factors (many of which are not actually the direct result of the brain injury, but related to the interaction of psychosocial influences) and should be thoroughly investigated in order to identify an appropriate intervention strategy. I would be happy to identify a potential referral source in your area if interested. I can be back channeled at kdavis@nhsltd.com. I would also be willing to provide resources that provide addition clarification.