- Kathryn Oden added an answer:4What are the biophysics or biomechanics of maxillofacial injuries in mTBI and its influence over cognitive performance & white matter tract integrity?
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.
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?Following
- Kavita Singh asked a question:OpenHow can I use PESS sequence for ipsilateral edematous region?
Am trying to study metabolite alteration from ipsilateral region after brain injury using PRESS sequence (TR/TE 2500/20 ms, 512 averages, spectral width of 4 kHz, 2048 data points). Am able to achieve FWHM of 5-9 but the spectral quality is poor post processing with low SNR =4.
Please help me the acquisition and post processing...Following
- Mohammad Yasin added an answer:2Does anyone know the half-life of leupeptin?
I would like to test leupeptin by injection intraperitoneally into rats who have received a brain injury, but need to know the half-life in order to determine the best dosing time-points. Any insight would be much appreciated!
Usually it is 7 min.Following
- Jens Bak Sommer added an answer:7Does anyone know how to deal with reduced motivation in the accelerating rotarod test?
We are currently using the accelerating rotarod test to assess vestibulomotor functioning following experimental brain injury in rats. In this regard, we have encountered that it can be very difficult to motivate animals to run on the rotarod: Some animals jump off the rod after a few seconds, whereas others seem to develop a strategy where they deliberately ‘fall’ off the rod in a more or less convincing manner after a relatively short time interval (e.g. 30 seconds). In both cases the performance/score does not appear to reflect the true vestibulomotor functioning of animals, and the performance of some animals vary significantly from trial to trial.
In order to establish a baseline performance level we have been giving animals 10 trials (5 days of 2 trials) before injury. Subsequently animals have been tested on the rotarod for 7 days (2 trials per day) post-injury. We are using a commercially available rotarod from PanLab/Harvard Apparatus (fall height 21 cm, rod diameter 60 mm, acceleration 4-40 rpm over 2 minutes).
If anyone has had similar experiences and has any ideas or advice on how to increase motivation in the rotarod test, it will be highly appreciated.
Thank you for your reply and data, Hanna. I will let you know how everything turned out after my next round of experiments.
Thanks again :0)
- Raoul Christian Sutter added an answer:6Can anyone recommend a validated observer-rated pain scale for nonverbal adult patients with a stroke/brain injury?
The setting is a neuro rehabilitation unit, patients aged 18 years and up. Thank you for your help.
Dear Krystal, perhaps this link and the attached paper will be of some help...
- Amanda Jane Tivnan added an answer:7Can anyone recommend a protocol for GLIOMA animal modelling ?
Has anyone tried GLIOMA animal modelling ? It will be really helpful if anyone could kindly suggest me a good protocol to follow.
I am looking for a collaborator to do GBM orthotopic animal model work please. I am a senior post-doctoral researcher in The Royal College of Surgeons in Ireland. I have several patient-derived GBM cell lines which are luciferase positive and would like to find an established group who are interested in collaborating for nanoparticle-mediated delivery mechanisms, the final part of my project please?
I look forward to hearing from you. My address is email@example.com
- Maurizio Iocco added an answer:4Have you ever seen in peripheral traumatic nerve injury a neurological repair without functional recovery?
I'm sure that in a few cases we have seen patient with persistent loss of function after a peripheral traumatic nerve lesion, but their conduction was normal.
Have you too?
Do you know why?
Yes I understand. It's true. But this is known for the central mechanism of recovery. but why in peripheral? I'm starting with a study about this problem.Following
- Nima Derakhshan added an answer:2Can glibenclamide be used as an adunctive therapy for cerebral edema in traumatic brain injury?The use of glibenclamide to control plasma glucose after TBI had no significant effect on patient outcome at discharge, but it could reduce the LOS-NICU (p<0.05). Glibenclamide also had no apparent effect on the presence of PSH in TBI patients with type 2 diabetes mellitus.Dear Kenneth
Corticosteroids are contraindicated in TBI as they resulted in worsening of outcomes in recent studies
It s a guideline according to evidence based dataFollowing
- Cory D Bovenzi added an answer:1What is the reason for projectile vomiting and nausea due to elevated intracranial pressure?Elevated intracranial pressure is often associated with vomiting. I would like to know how the pressure triggers the vomiting.
It may be due to transmitted pressure to the area postrema in the medulla, which is one area responsible for vomiting. The authors of Irwin and Rippe's Intensive Care Medicine agree.Following
- Pratyush Chaudhuri added an answer:6Management of post head-injury Bruxism.Patients with severe head injury esp , diffuse axonal injury may have associated bruxism which, to my experience, lasts for 10 -14 days. I have been studying these patients in recent years with trials of pramipexol and benzodiazapines. I have come across the botox inj studies as well. I wish to have suggestions from colleagues.
Yes dopamine agonist does work. I used pramipexole myself. Can you please give me your reference for the application of bromocriptine.
- Mustafa Volkan YAPRAKCI added an answer:1Hi everybody!This is a newly started group for everybody interested in neurotraumatology.
- Closed account added an answer:3Physician ScientistHallo I am new memeber of the groupWelcome!Following