Traumatic Brain Injury - Science topic

You can search ERABI (evidence-based review for acquired brain injury).

ERABI-Module-4-Motor-Sensory-V16.pdf (b-cdn.net)

The answer is no. The Tea Bag Index (TBI) was developed as a standardized method using standardized materials (i.e., Lipton tea). Even if you use the same type of tea (green and rooibos tea), the design, quantity and quality will differ from the standard Lipton tea. In other words, the results you get will not be useful because they are not comparable.

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.

Thank you professor, i will look for it.

regards

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.

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

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.

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?

William Kwan thank you very much!

Many thanks, Peter, that's a great help!

Following.

Good Answer Vladimir A. Kulchitsky

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

Please mention here...if you have found out any datasets for TBI CT scans

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!

...how long...years??

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.

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

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!

You can check out our contribution to satisfaction with life:

China put human brain genes in monkeys to study intelligence evolution.

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.

Have you tried with DWI sequence.

If the damage is in Gray matter, then you can go for FDG-PET.

Thanks

Hi -- I've published a couple papers on this. Langland-Hassan et al. (2015) "Inner speech deficits in people with aphasia," Frontiers in Psychology. Sharon Geva has also done good work on this--e.g., Geva et al. :

Mustafa Ali Khan Thank you for your reply but I would like to do voxel-based lesion symptom mapping(VLSM) so I need the image data. There are lots of publication focusing on VLSM from MR images but very few papers from CT images. I think this type of dataset will definitely benefit VLSM on clinical aspect.

please check the following sites:

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

Hello Prof Bryn

Projects seems nice and novel. I am interested in MS.

Studying the inflammatory phenomena provoked by progressive and recurrent traumatizations of brain tissues can no doubt further our understanding of unexplained neurodegenerative diseases/cryptic neuroinflammatory conditions. Which might hardly be the case the other way round!

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.

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.

Hello,

You can check these articles

Best wishes

Thank you very much dear Anup.

In a resource limiting setting:

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.

Stretch becomes shear when there is enough force. There is actually very little real evidence that axons re-grow within the CNS. Plasticity is a different phenomenon. In the peripheral nerve axons regenerate if they find a myelin sheet. If you want to study what happens to axons, you cannot first break them. If you cut the axons you end up studying the very complex remote consequences of denervation. One example would be crossed cerebellar diaschisis. My point is, that in TBI you always have a mix of tension, compression and tear. It is extremely difficult to determine what causes what. I think there is no good answer to your question.

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.

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.

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

An HMPAO perfusion SPECT scan is the best method.

Have a look at:

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

I agree with Shafagat Mahmudova good references. thanks

What are your dependent and independent measures?

Try Anthony David at the Maudsley London

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

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!

 Thank you for pointing out RBANS, your response was very helpful.

Hello Dushyant Kumar

please check the resources and one of the pdf is discussed in detail about TBI

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

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,

Depends on extent of edema and shift. Anterior temporal lobectomy or decompressive craniectomy appears to be the last resort.

Speak to these guys: http://www.ncbi.nlm.nih.gov/pubmed/27251042

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. 

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

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

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.

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.

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.

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. 

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.

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

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

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.

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.

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

GCS < 8

ICP >25 

OBLITERATION OF PEIMESENCEPHALIC CISTERNS IN THE CT SCAN

PATIENT  DECEREBRATE AND DECORTICATE POSTURING

MICRODIALYSIS- LACTATE:PYRUVATE RATIO > 23

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.

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?

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

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.

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.

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. 

1.  Stapert et al 2006 http://arnop.unimaas.nl/show.cgi?fid=4933

2. Silver et al, 2009 http://ajp.psychiatryonline.org/doi/pdf/10.1176/appi.ajp.2009.08111676

3. Bigler, 2013a http://journal.frontiersin.org/article/10.3389/fnhum.2013.00395/abstract

4. Le et al 2008 http://online.liebertpub.com/doi/abs/10.1089/neu.2008.0566

5.Spencer et al 2010 http://online.liebertpub.com/doi/abs/10.1089/neu.2008.0566

6. Shenton et al 2012 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3803157/

7. Bigler , 2013b http://www.mccauslandcenter.sc.edu/CRNL/sw/tbi/7/2013_BiglerA.pdf

8. Mayor et al, 2010 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830922/

9. Irimia et al 2012 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757727/

10. Croall et al, 2014 http://www.neurology.org/content/early/2014/07/16/WNL.0000000000000666

11. Lo et al, 2009 http://www.ncbi.nlm.nih.gov/pubmed/19346863

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. 

von Steinbuchel, N., Wilson, L., Gibbons, H., Hawthorne, G., Hofer, S., Schmidt, S., . . . Force, Q. T. (2010). Quality of Life after Brain Injury (QOLIBRI): scale development and metric properties. J Neurotrauma, 27(7), 1167-1185. doi: 10.1089/neu.2009.1076

von Steinbuchel, N., Wilson, L., Gibbons, H., Hawthorne, G., Hofer, S., Schmidt, S., . . . Force, Q. T. (2010). Quality of Life after Brain Injury (QOLIBRI): scale validity and correlates of quality of life. J Neurotrauma, 27(7), 1157-1165. doi: 10.1089/neu.2009.1077

Valovich McLeod, T. C., Bay, R. C., Parsons, J. T., Sauers, E. L., & Snyder, A. R. (2009). Recent injury and health-related quality of life in adolescent athletes. J Athl Train, 44(6), 603-610. doi: 10.4085/1062-6050-44.6.603

Siponkoski, S. T., Wilson, L., von Steinbuchel, N., Sarajuuri, J., & Koskinen, S. (2013). Quality of life after traumatic brain injury: Finnish experience of the QOLIBRI in residential rehabilitation. J Rehabil Med, 45(8), 835-842. doi: 10.2340/16501977-1189

Hawthorne, G., Kaye, A. H., Gruen, R., Houseman, D., & Bauer, I. (2011). Traumatic brain injury and quality of life: initial Australian validation of the QOLIBRI. J Clin Neurosci, 18(2), 197-202. doi: 10.1016/j.jocn.2010.06.015

Thank you for your kind suggestions, Dr Altay. Will surely check the paper out.

I am currently working on how certain genetic predispositions actually affects the events that occurs in between the primary insult and the secondary trauma in brain injury. For example, rs6265 of BDNF has been implicated to negatively affect certain psychiatric conditions. However, not much work has been done in mTBI, especially with regards to its influence on microstructural changes across different time intervals. While working on the DTI results, we realised that some quarter of our patients with vasogenic edema and astrogliosis (evinced in the preliminary results) performing poorly in neurocognitive assessments across the time points in comparison to others from the same mTBI group. We would like to understand why..

(I posted the question in order to encourage people to share their opinions and engage one another in the effort of advancing the limited knowledge on the subject matter.)

Studies have shown that the 1st 7-10 days is the period of greatest risk for incurring a second concussion.  In mild TBI there is cellular damage as well as micro-structural damage, and it is imperative that we keep external forces to the brain at a minimum to allow healing.  Studies are showing that the younger children require longer time to recover and we need to be conservative with our return to sports and recreational activity that has the potential to cause re-injury.  Best NOT TO SHAKE THE HEAD!!

you're welcome

Assessment of reactivity can be the first step in approaching the relations among cerebral blood flow, oxygen delivery, demand, and cellular metabolism.

interesting article to read

Dear Vigneswaran Veeramuthu,

You find from here:

Yes, for example in some sports (e.g. American football) the measurement of linear and angular acceleration through technologies fitted to helmets to identify concussion or mild TBI. There is also a body of research findings since the 1960s concerning the biomechanics involved in TBI, which may be useful to consider.