Posts Tagged brain injury

[BLOG POST] Flying with a brain injury: my first long flight – Finding a new normal

Flying is my least favourite mode of transportation. Unfortunately it’s also the most convenient way to travel outside of Europe.

After my brain injury I was very curious about whether or not I’d still be able to fly (by myself). This called for an experiment.

Trying out flying

My first flight was a year and a half after my brain injury. At that time I could handle far less compared to the situation now. I had far less energy and got overstimulated very easily. Or maybe I had yet to discover how I should handle the ‘new me’.

So I avoided places with a lot of people. As fifteen minutes in a busy place would deteriorate my speech, thinking and balance quickly. Flying thus was written of in advance.

Luckily someone told me about the special assistence you can request when you plan to fly. This service makes it easier for people with any kind of disability to travel by plane. Once requested in advance, someone will escort you all the way into the plane. Which means that you get a lot faster through the airport and can save some precious energy. This service made flying suddenly a possibility.

And as a result I had two succesful flights within Europe. Which meant that it was time for the next step. To take a long flight and to try it without any kind of assistance.

A ten hour flight

That long flight was my flight to Sri Lanka last week. This time, not the airport but the flight itself was the most challenging. In the airport I had my earplugs, noise cancelling headphones and sunglasses and could hide out in a quiet corner. I even made a reservation for an airport lounge to rest in, which almost made me forget I was at an airport.

In the plane however, you can’t leave. Blocking out the world is a whole lot harder if there’s nowhere for you to go. This made the flight challenging, thought the last three hours of turbulance might also be to blame. Still I learned some lessons for my next flight in five weeks.

Know your triggers

I always find travel days extremely stressful. Nine out of ten times this culminates in a panic attack. This time was no different. Thankfully I recognised I was having a panic attack early on, so I could do something about it.

Follow your gut

If you notice that you stress yourself out over something, try and do something about it. I kept chaecking my watch every other minute, because I was afraid to be late. After an hour of annoying myself I finally decided to just go to the airport way too early. Looking back I should have done that earlier.

Plan your route

Nowadays, I think you can find the map of almost all airports online. This means that you can plan where to go in advance. Knowing where the lounges, quiet areas or prayer rooms are located beforehand can give you some piece of mind. Once you’ve passed security at the airport you already know the shortest way to where you plan to rest.

Keep a choice of distractions ready

Once you’re seated in the plane, it’s a matter of sitting it through. Of waiting until the plane has landed and you can get off. I discovered that I can’t read or watch tv on a plane. My mp3 player is therefore filled with different kinds of music. Music to sleep, to distract or to cancel out other noises. Make sure you have the option of distractions for the duration of the flight.

Keep yourself hydrated

Any time you get offered a drink on the plane, take it. Not only will it help you to stay hydrated (so don’t pick an alcoholic drink) it’ll force you to go to the toilet. In other words to stand up and walk around.

After care

The second or third day after the flight, I’ll feel the consequences. So listen to your body. If you need to sleep for 12 hours, do that. If you crave sugary or salty snacks, have those. Flying is hard and challenging, so take some recovery days into account and allow yourself some rest.

– I can only speak from my own exprience, so do check with your doctor if you have specific requirements to take into account when flying –

What do you do when you fly? Do you have or need something special that really helps you?

via Flying with a brain injury: my first long flight – Finding a new normal


, , ,

Leave a comment

[BLOG POST] Parenting After Brain Injury – Neuro Landscape


While there are no prerequisites for the job, parenthood is a lifelong responsibility. It is also one of the most fulfilling and important roles a person can have in life. Brain injury, unfortunately, impacts individuals without regard to their roles and responsibilities.

Persons with brain injury are challenged in their ability to care for themselves, much less others, making parenting more difficult. Yet, in order to achieve long-term success post-injury, family reintegration, including parenting, is imperative. And the best way to achieve this is through skill redevelopment during postacute rehabilitation.

The Basics Still Apply, Before and After Brain Injury

Parenting requires the ability to not only care for oneself, but to do so often in deference to caring for children. Parents are frequently required to subjugate their needs and wishes to the importance of providing for the well-being, nurturing, education, safety, development, and future of their children.

This requires a mindful approach, planning with a spouse or partner, or managing alone with family and friends to provide for housing, food, clothing, and education all the while seeking to instill family and societal values. Most parents want their children to be safe and to have a future that is the same as or better than their own.

Raising children presents a range of personal challenges to most parents. It may require developing a willingness for selflessness while acquiring skills as a teacher, mentor, role model, and disciplinarian, at least. Many couples acknowledge that arriving at a parenting style can be arduous and the source of conflict in their relationship as they negotiate stylistic differences and determine and articulate behavioral, educational, value, and moral expectations for their children.

Relearning Parenting Skills is Vital to Family Integration

After brain injury, however, individuals tend to become more focused on themselves, and fail to provide the same kind of parenting approach/skills as they exerted prior to injury. They are likely to be much less involved in child rearing, in general, failing to participate in determining, communicating, and facilitating goals for their children. These responsibilities either are not met well, or fall entirely to a non-injured spouse, partner, or family member.

Active discussions must be undertaken with an individual and/or couple to raise awareness of the importance of assessment and intervention for parenting skills, and to actively intervene to redevelop such skills and focus within the family. Family members must be relied upon to build an understanding of parenting skills and styles prior to injury as well as parenting-related family dynamics so as to serve as goals for treatment.

These efforts must focus not only on reacquisition of parenting styles and skills, but also on parental engagement with children in accordance with the manner in which they engaged prior to injury. Finally, teaching must include knowledge of common reactions children may have to the temporary or permanent loss of a parent to injury. Counseling can be extremely effective in raising awareness of these issues and changing behaviors within a family system. Counseling can incorporate other family members such as spouses/partners, children themselves, or key extended family members with meaningful insights such as close aunts/uncles or grandparents. Re-engagement within a family system to the various roles one played prior to injury is critical to the long-term success of family reintegration.


via Parenting After Brain Injury – Neuro Landscape

, ,

Leave a comment

[BLOG POST] 10 small things you can do to help someone with a brain injury

helping someone

Five years ago I had no idea what a brain injury was, let alone how to help someone with a brain injury. I discovered that a lot of people don’t know what it means to live with a brain injury or how they can help.

Nowadays, people regularly tell me to let them know if they can help me with anything. I never know how to respond to this offer. Were they just being polite or did they mean it? What can or can’t I ask of someone? When does my request turns into a burden? What kind of help do I want?

However, the truth of the matter is that people definitely can help. Especially in social settings. By trial and error I’ve learned a couple of things that help me. Thus I thought it would be a good idea to put them into a list. A list of ten things with which my close friends and family members help me most often. Whenever someone offers to help me in the future, I’ll just point them to this list and let them pick and choose.

I hope this list can also help or inspire you in some way. A small disclaimer though, every brain injury is unique. I can only speak from my experience, but what works for me doesn’t have to work for others.  If you have any additions to this list please let me know! I can always write a later update.

pin help someone with brain innjury

10 tips to help someone with a brain injury

  1. Get in touch
    If I don’t do something straight away and or write it down, I’ll likely forget doing it at all. I’ll just get distracted by everyday things and forget to get in touch or to plan a get together. So get in touch with us* if you haven’t heard from us in a while.
    * I kept struggling with I vs. we vs. you, so whenever I use ‘we’ or ‘us’ in this list, I mean we who have a brain injury.
  1. Bringing food
    The act of cooking or doing groceries are both exhausting. It therefore can really help if you can pick up some groceries or maybe even bring over that’s already prepared.
  1. No background music
    I used to love to have some music playing in the background. Not any more though, as I can’t tune it out. This means that it takes a lot of attention and energy if I also have to try and stay focused on the conversation. It helps a lot if you have no music (or clocks that tick loudly) playing.
  1. Providing a quiet place
    After forty-five minutes of talking I need to take a small break. To be one my own for ten minutes to process all the information and give my brain a chance to catch up. If you can point us to a certain room or place where we can retreat to so we can give our brain a break.
  1. Choosing where to sit
    If we’re going somewhere, I’m mainly paying attention to all the things I’d like to avoid. Things like speakers, harsh lighting, striped wallpaper, small children and large groups. Just about everything that provides a ton of auditory or visual stimuli. So if you can let us decide where we’d like to sit, we can stay out longer.
  1. Decide when to leave
    I love meeting with people and like to do that as long as possible. I’d only notice afterwards how far I’ve exceeded my limits. Rather than waiting for us to tell you to go, it therefore helps if you leave the moment you notice that we’re getting tired.
  1. Ask how today is
    People always ask how you are doing and I never know how to respond. It’s one of those open ended question where I never know what they want to know exactly and how I should respond. So ask how today is going. This is a much more defined questions, which is easier to answer.
  1. Don’t make it too complicated
    Don’t use too much imagery or abstract thinking. Whenever this happens I will be so busy ‘translating’ whatever you’re trying to say, that I lose the tread of the conversation. So keep it simple.
  1. See the progress
    It’s easier for me to compare my life ‘before brain injury’ with life ‘after brain injury’. Which isn’t helpful at all. If you see improvement compared to the last time you saw us, please let us know! It helps being made aware of the progress we have made.
  1. Be patient 
    Sometime we have trouble articulating. Either with putting our thoughts into words or finding a specific word. In that case, please be patient and wait for our brains to catch up. Eventually we will manage. If we suddenly start to cry or get angry, please don’t take it personally and try to stay patient. That’s a sure sign that we’ve reached our limits and need to sleep.

I hope this can help you as well. And to my dear friends and family, thank you for doing your best to accommodate the new me.

Do you use some of these or do you struggle with other things? If you have any additions to this list please let me know!

via 10 small things you can do to help someone with a brain injury – Finding a new normal


Leave a comment

[Abstract+References] Evidence for Training-Dependent Structural Neuroplasticity in Brain-Injured Patients: A Critical Review

Acquired brain injury (ABI) is associated with a range of cognitive and motor deficits, and poses a significant personal, societal, and economic burden. Rehabilitation programs are available that target motor skills or cognitive functioning. In this review, we summarize the existing evidence that training may enhance structural neuroplasticity in patients with ABI, as assessed using structural magnetic resonance imaging (MRI)–based techniques that probe microstructure or morphology. Twenty-five research articles met key inclusion criteria. Most trials measured relevant outcomes and had treatment benefits that would justify the risk of potential harm. The rehabilitation program included a variety of task-oriented movement exercises (such as facilitation therapy, postural control training), neurorehabilitation techniques (such as constraint-induced movement therapy) or computer-assisted training programs (eg, Cogmed program). The reviewed studies describe regional alterations in white matter architecture and/or gray matter volume with training. Only weak-to-moderate correlations were observed between improved behavioral function and structural changes. While structural MRI is a powerful tool for detection of longitudinal structural changes, specific measures about the underlying biological mechanisms are lacking. Continued work in this field may potentially see structural MRI metrics used as biomarkers to help guide treatment at the individual patient level.

1. O’Rance, L, Fortune, N. Disability in Australia: Acquired Brain Injury. Canberra, AustraliaAustralian Institute of Health and Welfare2007:124Google Scholar
2. Rabinowitz, A, Levin, HS. Cognitive sequale of traumatic brain injury. Psychiatr Clin North Am. 2014;37:111Google ScholarCrossrefMedline
3. Kuhtz-Buschbeck, JP, Hoppe, B, Gölge, M, Dreesmann, M, Damm-Stünitz, U, Ritz, A. Sensorimotor recovery in children after traumatic brain injury: analyses of gait, gross motor, and fine motor skills. Dev Med Child Neurol. 2003;45:821828Google ScholarCrossrefMedline
4. Hayes, JP, Bigler, ED, Verfaellie, M. Traumatic brain injury as a disorder of brain connectivity. J Int Neuropsychol Soc. 2016;22:120137. doi:10.1017/S1355617715000740. Google ScholarCrossrefMedline
5. Drijkoningen, D, Caeyenberghs, K, Vander Linden, C, Van Herpe, K, Duysens, J, Swinnen, SP. Associations between muscle strength asymmetry and impairments in gait and posture in young brain-injured patients. J Neurotrauma. 2015;32:13241332. doi:10.1089/neu.2014.3787. Google ScholarCrossrefMedline
6. Nocentini, U, Bozzali, M, Spanò, B. Exploration of the relationships between regional grey matter atrophy and cognition in multiple sclerosis. Brain Imaging Behav. 2014;8:378386. doi:10.1007/s11682-012-9170-7. Google ScholarCrossrefMedline
7. Hulkower, MB, Poliak, DB, Rosenbaum, SB, Zimmerman, ME, Lipton, ML. A decade of DTI in traumatic brain injury: 10 years and 100 articles later. AJNR Am J Neuroradiol. 2013;34:20642074. doi:10.3174/ajnr.A3395. Google ScholarCrossrefMedline
8. Caeyenberghs, K, Wenderoth, N, Smits-Engelsman, BC, Sunaert, S, Swinnen, SP. Neural correlates of motor dysfunction in children with traumatic brain injury: exploration of compensatory recruitment patterns. Brain. 2009;132(pt 3):684694Google ScholarCrossrefMedline
9. Chen, H, Epstein, J, Stern, E. Neural plasticity after acquired brain injury: evidence from functional neuroimaging. PM R. 2010;2(12 suppl 2):S306S312. doi:10.1016/j.pmrj.2010.10.006. Google ScholarCrossrefMedline
10. Choo, PL, Gallagher, HL, Morris, J, Pomeroy, VM, van Wijck, F. Correlations between arm motor behavior and brain function following bilateral arm training after stroke: a systematic review. Brain Behav. 2015;5:e00411. doi: 10.1002/brb3.411. Google ScholarCrossrefMedline
11. Matthews, PM, Johansen-Berg, H, Reddy, H. Non-invasive mapping of brain functions and brain recovery: applying lessons from cognitive neuroscience to neurorehabilitation. Restor Neurol Neurosci. 2004;22:245260Google ScholarMedline
12. Prosperini, L, Piattella, MC, Giannì, C, Pantano, P. Functional and structural brain plasticity enhanced by motor and cognitive rehabilitation in multiple sclerosis. Neural Plast. 2015;2015:481574. doi:10.1155/2015/481574. Google ScholarCrossrefMedline
13. Reid, LB, Boyd, RN, Cunnington, R, Rose, SE. Interpreting intervention induced neuroplasticity with fMRI: the case for multimodal imaging strategies. Neural Plast. 2016;2016:2643491. doi:10.1155/2016/2643491.Google ScholarCrossrefMedline
14. Richards, LG, Stewart, KC, Woodbury, ML, Senesac, C, Cauraugh, JH. Movement-dependent stroke recovery: a systematic review and meta-analysis of TMS and fMRI evidence. Neuropsychologia. 2008;46:311Google ScholarCrossrefMedline
15. Mechelli, A, Crinion, JT, Noppeney, U. Neurolinguistics: structural plasticity in the bilingual brain. Nature. 2004;431:757. doi:10.1038/431757a. Google ScholarCrossrefMedline
16. Takeuchi, H, Sekiguchi, A, Taki, Y. Training of working memory impacts structural connectivity. J Neurosci. 2010;30:32973303. doi:10.1523/JNEUROSCI.4611-09.2010. Google ScholarCrossrefMedline
17. van Tulder, M, Furlan, A, Bombardier, C, Bouter, L; Editorial Board of the Cochrane Collaboration Back Review Group. Updated method guidelines for systematic reviews in the cochrane collaboration back review group. Spine (Phila Pa 1976). 2003;28:12901299Google ScholarCrossrefMedline
18. Fritz, NE, Cheek, FM, Nichols-Larsen, DS. Motor-cognitive dual-task training in persons with neurologic disorders: a systematic review. J Neurol Phys Ther. 2015;39:142153. doi:10.1097/NPT.0000000000000090. Google ScholarCrossrefMedline
19. Guzmán, J, Esmail, R, Karjalainen, K, Malmivaara, A, Irvin, E, Bombardier, C. Multidisciplinary rehabilitation for chronic low back pain: systematic review. BMJ. 2001;322:15111516Google ScholarCrossrefMedline
20. Karjalainen, K, Malmivaara, A, van Tulder, M. Multidisciplinary biopsychosocial rehabilitation for subacute low back pain in working-age adults: a systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine (Phila Pa 1976). 2001;26:262269Google ScholarCrossrefMedline
21. Gauthier, LV, Taub, E, Perkins, C, Ortmann, M, Mark, VW, Uswatte, G. Remodeling the brain: plastic structural brain changes produced by different motor therapies after stroke. Stroke. 2008;39:15201525. doi:10.1161/STROKEAHA.107.502229. Google ScholarCrossrefMedline
22. Schlaug, G, Marchina, S, Norton, A. Evidence for plasticity in white-matter tracts of patients with chronic Broca’s aphasia undergoing intense intonation-based speech therapy. Ann N Y Acad Sci. 2009;1169:385394. doi:10.1111/j.1749-6632.2009.04587.x. Google ScholarCrossrefMedline
23. Breier, J, Juranek, J, Papanicolaou, A. Changes in maps of language function and the integrity of the arcuate fasciculus after therapy for chronic aphasia. Neurocase. 2011;17:506517. doi:10.1080/13554794.2010.547505. Google ScholarCrossrefMedline
24. Caria, A, Weber, C, Brötz, D. Chronic stroke recovery after combined BCI training and physiotherapy: a case report. Psychophysiology. 2011;48:578582. doi:10.1111/j.1469-8986.2010.01117.x. Google ScholarCrossrefMedline
25. Nordvik, JE, Schanke, AK, Walhovd, K, Fjell, A, Grydeland, H, Landrø, NI. Exploring the relationship between white matter microstructure and working memory functioning following stroke: a single case study of computerized cognitive training. Neurocase. 2012;18:139151. doi:10.1080/13554794.2011.568501.Google ScholarCrossrefMedline
26. Borstad, AL, Bird, T, Choi, S, Goodman, L, Schmalbrock, P, Nichols-Larsen, DS. Sensorimotor training induced neural reorganization after stroke: a case series. J Neurol Phys Ther. 2013;37:2736. doi:10.1097/NPT.0b013e318283de0d. Google ScholarCrossrefMedline
27. Lazaridou, A, Astrakas, L, Mintzopoulos, D. Diffusion tensor and volumetric magnetic resonance Imaging using an MR-compatible hand-induced robotic device suggests training-induced neuroplasticity in patients with chronic stroke. Int J Mol Med. 2013;32:9951000. doi:10.3892/ijmm.2013.1476. Google ScholarCrossrefMedline
28. Särkämö, T, Ripollés, P, Vepsäläinen, H. Structural changes induced by daily music listening in the recovering brain after middle cerebral artery stroke: a voxel-based morphometry study. Front Hum Neurosci. 2014;8:245. doi:10.3389/fnhum.2014.00245. Google ScholarCrossrefMedline
29. Wan, CY, Zheng, X, Marchina, S, Norton, A, Schlaug, G. Intensive therapy induces contralateral white matter changes in chronic stroke patients with Broca’s aphasia. Brain Lang. 2014;136:17. doi:10.1016/j.bandl.2014.03.011. Google ScholarCrossrefMedline
30. Fan, YT, Lin, KC, Liu, HL, Chen, YL, Wu, CY. Changes in structural integrity are correlated with motor and functional recovery after post-stroke rehabilitation. Restor Neurol Neurosci. 2015;33:835844. doi:10.3233/RNN-150523. Google ScholarCrossrefMedline
31. Young, BM, Stamm, JM, Song, J. Brain-computer interface training and stroke affects patterns of brain-behavior relationships in corticospinal motor fibers. Front Hum Neurosci. 2016;10:457Google ScholarCrossrefMedline
32. Wilkins, KB, Owen, M, Ingo, C, Carmona, C, Dewald, J, Yao, J. Neural plasticity in moderate to severe chronic stroke following a device-assisted task-specific arm/hand intervention Front Neurol. 2017;8:284. doi:10.33389/fneur.2017.00284. Google ScholarCrossrefMedline
33. Yang, HE, Kyeong, S, Lee, SH. Structural and functional improvements due to robot-assisted gait training in the stroke-injured brain. Neurosci Lett. 2017;637:114119Google ScholarCrossrefMedline
34. Ibrahim, I, Tintera, J, Skoch, A. Fractional anisotropy and mean diffusivity in the corpus callosum of patients with multiple sclerosis: the effect of physiotherapy. Neuroradiology. 2011;53:917926. doi:10.1007/s00234-011-0879-6. Google ScholarCrossrefMedline
35. Filippi, M, Riccitelli, G, Mattioli, F. Multiple sclerosis: effects of cognitive rehabilitation on structural and functional MR imaging measures—an explorative study. Radiology. 2012;262:932940. doi:10.1148/radiol.11111299. Google ScholarCrossrefMedline
36. Bonzano, L, Tacchino, A, Brichetto, G. Upper limb motor rehabilitation impacts white matter microstructure in multiple sclerosis. Neuroimage. 2014;90:107116. doi:10.1016/j.neuroimage.2013.12.025. Google ScholarCrossrefMedline
37. Prosperini, L, Fanelli, F, Petsas, N. Multiple sclerosis: changes in microarchitecture of white matter tracts after training with a video game balance board. Radiology. 2014;273:529538. doi:10.1148/radiol.14140168. Google ScholarCrossrefMedline
38. Rasova, K, Prochazkova, M, Tintera, J, Ibrahim, I, Zimova, D, Stetkarova, I. Motor programme activating therapy influences adaptive brain functions in multiple sclerosis: clinical and MRI study. Int J Rehabil Res. 2015;38:4954. doi:10.1097/MRR.0000000000000090. Google ScholarCrossrefMedline
39. Ernst, A, Sourty, M, Roquet, D. Functional and structural cerebral changes in key brain regions after facilitation programme for episodic future thought in relapsing-remitting multiple sclerosis patients. Brain Cogn. 2016;105:3445Google ScholarCrossrefMedline
40. Cruickshank, TM, Thompson, JA, Domínguez, D. The effect of multidisciplinary rehabilitation on brain structure and cognition in Huntington’s disease: an exploratory study. Brain Behav. 2015;5:e00312. doi:10.1002/brb3.312. Google ScholarCrossrefMedline
41. Metzler-Baddeley, C, Cantera, J, Coulthard, E, Rosser, A, Jones, DK, Baddeley, RJ. Improved executive function and callosal white matter microstructure after rhythm exercise in Huntington’s disease. J Huntingtons Dis. 2014;3:273283. doi:10.3233/JHD-140113. Google ScholarCrossrefMedline
42. Sehm, B, Taubert, M, Conde, V. Structural brain plasticity in Parkinson’s disease induced by balance training. Neurobiol Aging. 2014;35:232239. doi:10.1016/j.neurobiolaging.2013.06.021. Google ScholarCrossrefMedline
43. Díez-Cirarda, M, Ojeda, N, Peña, J. Increased brain connectivity and activation after cognitive rehabilitation in Parkinson’s disease: a randomized controlled trial. Brain Imaging Behav. 2017;11:16401651Google ScholarCrossrefMedline
44. Burciu, RG, Fritsche, N, Granert, O. Brain changes associated with postural training in patients with cerebellar degeneration: a voxel-based morphometry study. J Neurosci. 2013;33:45944604. doi:10.1523/JNEUROSCI.3381-12.2013. Google ScholarCrossrefMedline
45. Han, K, Davis, RA, Chapman, SB, Krawczyk, DC. Strategy-based reasoning training modulates cortical thickness and resting-state functional connectivity in adults with chronic traumatic brain injury. Brain Behav. 2017;7:e00687. doi:10.1002/brb3.687. Google ScholarCrossrefMedline
46. Cohen, J. Statistical Power Analysis for the Behavioral Sciences. Hilsdale, NJLawrence Earlbaum1988Google Scholar
47. Borenstein, M, Hedges, LV, Higgins, JPT, Rothstein, HR. Multiple outcomes or time-points within a study. In: Borenstein, M, ed. Introduction to Meta-Analysis. Chichester, EnglandWiley2009:225238Google ScholarCrossref
48. Thomas, C, Baker, CI. Teaching an adult brain new tricks: a critical review of evidence for training-dependent structural plasticity in humans. Neuroimage. 2013;73:225236. doi:10.1016/j.neuroimage.2012.03.069. Google ScholarCrossrefMedline
49. Smith, S, Rao, A, De Stefano, N. Longitudinal and cross-sectional analysis of atrophy in Alzheimer’s disease: cross-validation of BSI, SIENA and SIENAX. Neuroimage. 2007;36:12001206. doi:10.1016/j.neuroimage.2007.04.035. Google ScholarCrossrefMedline
50. Heiervang, E, Behrens, TE, Mackay, CE, Robson, MD, Johansen-Berg, H. Between session reproducibility and between subject variability of diffusion MR and tractography measures. Neuroimage. 2006;33:867877. doi:10.1016/j.neuroimage.2006.07.037. Google ScholarCrossrefMedline
51. Wakana, S, Caprihan, A, Panzenboeck, MM. Reproducibility of quantitative tractography methods applied to cerebral white matter. Neuroimage. 2007;36:630644. doi:10.1016/j.neuroimage.2007.02.049. Google ScholarCrossrefMedline
52. Scholz, J, Klein, MC, Behrens, TE, Johansen-Berg, H. Training induces changes in white-matter architecture. Nat Neurosci. 2009;12:13701371. doi:10.1038/nn.2412. Google ScholarCrossrefMedline
53. Taubert, M, Draganski, B, Anwander, A. Dynamic properties of human brain structure: learning-related changes in cortical areas and associated fiber connections. J Neurosci. 2010;30:1167011677. doi:10.1523/JNEUROSCI.2567-10.2010. Google ScholarCrossrefMedline
54. Hofstetter, S, Tavor, I, Tzur Moryosef, S, Assaf, Y. Short-term learning induces white matter plasticity in the fornix. J Neurosci. 2013;33:1284411280. doi:10.1523/JNEUROSCI.4520-12.2013. Google ScholarCrossrefMedline
55. Cercignani, M, Bammer, R, Sormani, MP, Fazekas, F, Filippi, M. Inter-sequence and inter-imaging unit variability of diffusion tensor MR imaging histogram-derived metrics of the brain in healthy volunteers. AJNR Am J Neuroradiol. 2003;24:638643Google ScholarMedline
56. Price, R, Axel, L, Morgan, T. Quality assurance methods and phantoms for magnetic resonance imaging: report of AAPM Nuclear Magnetic Resonance Task Group No. 1. Med Phys. 1990;17:287295. doi:10.1118/1.596566. Google ScholarCrossrefMedline
57. Bookstein, FL. “Voxel-based morphometry” should not be used with imperfectly registered images. Neuroimage. 2001;14:14541462Google ScholarCrossrefMedline
58. Thompson, WK, Holland, D; Alzheimer’s Disease Neuroimaging Initiative. Bias in tensor based morphometry Stat-ROI measures may result in unrealistic power estimates. Neuroimage. 2011;57:14. doi:10.1016/j.neuroimage.2010.11.092. Google ScholarCrossrefMedline
59. Zatorre, RJ, Fields, RD, Johansen-Berg, H. Plasticity in gray and white: neuroimaging changes in brain structure during learning. Nat Neurosci. 2012;15:528536. doi:10.1038/nn.3045. Google ScholarCrossrefMedline
60. Eriksson, S, Free, S, Thom, M. Quantitative grey matter histological measures do not correlate with grey matter probability values from in vivo MRI in the temporal lobe. J Neurosci Methods. 2009;181:111118. doi:10.1016/j.jneumeth.2009.05.001. Google ScholarCrossrefMedline
61. Jones, DK, Knösche, TR, Turner, R. White matter integrity, fiber count, and other fallacies: the do’s and don’ts of diffusion MRI. Neuroimage. 2011;73:239254. doi:10.1016/j.neuroimage.2012.06.081. Google ScholarCrossref
62. Jeurissen, B, Leemans, A, Jones, DK, Tournier, JD, Sijbers, J. Probabilistic fiber tracking using the residual bootstrap with constrained spherical deconvolution. Hum Brain Mapp. 2011;32:461479. doi:10.1002/hbm.21032. Google ScholarCrossrefMedline
63. Caeyenberghs, K, Metzler-Baddeley, C, Foley, S, Jones, DK. Dynamics of the human structural connectome underlying working memory training. J Neurosci. 2016;36:40564066. doi:10.1523/jneurosci.1973-15.2016. Google ScholarCrossrefMedline
64. Metzler-Baddeley, C, Foley, S, de Santis, S. Dynamics of white matter plasticity underlying working memory training: multimodal evidence from diffusion MRI and relaxometry. J Cogn Neurosci. 2017;29:15091520. doi:10.1162/jocn_a_01127. Google ScholarCrossrefMedline
65. Assaf, Y, Basser, PJ. Composite hindered and restricted model of diffusion (CHARMED) MR imaging of the human brain. Neuroimage. 2005;27:4858. doi:10.1016/j.neuroimage.2005.03.042. Google ScholarCrossrefMedline
66. Deoni, SC, Rutt, BK, Jones, DK. Investigating exchange and multicomponent relaxation in fully-balanced steady-state free precession imaging. J Magn Reson Imaging. 2008;27:14211429. doi:10.1002/jmri.21079. Google ScholarCrossrefMedline

via Evidence for Training-Dependent Structural Neuroplasticity in Brain-Injured Patients: A Critical Review – Karen Caeyenberghs, Adam Clemente, Phoebe Imms, Gary Egan, Darren R. Hocking, Alexander Leemans, Claudia Metzler-Baddeley, Derek K. Jones, Peter H. Wilson, 2018

, , , ,

Leave a comment

[WEB SITE] Featured Article: Comprehending Aggressive Behavior Following A Brain Injury: An Explanatory Framework for Neurobehavior

Jeff Kupfer, Peter R. Killeen, & Randall D. Buzan

“Why is he behaving this way?” is the central question caregivers and family members of patients with Traumatic Brain Injury (TBI) pose, pointing to extreme agitation, antisocial behavior, insensitive interactions, or other manifestations of his condition. Our clinical team gives various answers from the varied perspectives and expertise of members. Accurate though these explanations are, they often don’t hang together, and often don’t satisfy the questioner. What is wrong with our explanations? Was something lost in translation of scientific jargon? Perhaps some features that could provide a complete explanation were omitted. This paper presents a framework for explanations that permits a more integrated and complete picture, and reminds practitioners of aspects that should be included in a thorough understanding of behavior after TBI.

PART ONE:  Explaining a behavioral event: “How did that lamp break?”

Consider the following family situation: a Sunday afternoon family brunch, post-meal conversation around the dining table. Suddenly we hear the laughter of children, footsteps running down the stairs and through the living room. The front door slams, followed by the sound of a lamp crashing to the floor in the foyer. Table 1 organizes the diversity of explanations by the family members for this household accident.

Table 1. Dialogue amongst family members following a behavior event.

Event is Described Focus “Cause”
Focus on the behavior
“I’ve told them not to run in the house” Running describes the form of behavior Formal
“Joey led the charge out the front door” Trigger was Joey Efficient
“They were bored in here with all the adult talk” State of the system: Arousal ready for displacement Material
“And they were eager to play with that new hoop set you got for Joey’s birthday.” Purpose, function, Final
“Well let’s not forget the sugar high from that excellent dessert” State of the system: Arousal ready for displacement Material
Focus on environment
“It’s smithereens now—no way even grandpa could fix it” Describes current status Formal
“It’s not completely their fault, Helen. That old lamp was pretty tippy: A strong wind would knock it over” Many possible ways for it to break Efficient
“It was Joey who bumped it over” The particular trigger that tripped it Efficient
“Helen! It was missing its fourth leg!!” Lack of structural integrity Material
“Joseph, I think you loosened it just to make this happen, given how you hated that old lamp!” The reason the leg was loosened and broken off Final

We see that an unexceptional event may be examined from various points of view, all which may be correct. Similarly, brain and behavior sciences provide scientific explanations of events from various points of view, but even they typically fall into several classes. These are the classes of explanation identified by Aristotle that are required before we may claim to truly understand a phenomenon (Hocutt, 1974).

Aristotle’s framework for explanations

Aristotle’s name for these classes of explanation was mistranslated as “Causes”, a proper title in modern parlance for only one type (efficient cause). This led to his schema being dismissed as confusing and even teleological. A better class name is reasons for, or becauses (Killeen, 2001). Aristotle’s framework addresses the broad range of possible explanations for any phenomenon, and coordinates these explanations to arrive at a more integrated understanding. We can utilize this model to describe behavior following a brain injury.

Formal causes (names, forms, and models) are the ways we talk about, represent and describe events. They translate the essentials of their relevant aspects into words, numbers or diagrams. Simple descriptions, such as the example above (“running resulted in the lamp breaking”) can get the formal ball rolling, but these can be extended to include models, metaphors, logical phrases, equations, schematics, blueprints, or flowcharts that help us organize, summarize, and communicate phenomena. Behavioral experts use DSM diagnoses as “formal causes” to describe and explain patient behavior, and brain injury professionals use the Glasgow Coma Scale or Ranchos Los Amigos Scale as formal descriptors of a patient’s condition. Physicists and astronomers utilize differential equations as their formal models. Behavior analysts describe behavior with three-and four-term contingencies for simple and conditional discriminations (antecedent, behavior, consequence, A-B-C).

Efficient causes (triggers) refer to the necessary and sufficient conditions to bring about a change in state (factors triggering an event). These are commonly what are meant by “causes” (Joey’s running in the house caused the lamp to fall [when he careened into it]). Efficient causes of reckless behavior identify events or people that trigger action, as well as events that can minimize or prevent its occurrences. Efficient causes are conditions sufficient to trigger the phenomenon being explained that were operative at the critical moment. There may be many possible sufficient conditions, just as there are many possible roads to Rome; functional analyses clarify which ones were operative in a particular case. Necessary causes are usually invoked to explain failures of expected outcomes: Why didn’t the car start? It needed gas (electricity, functional starter, etc.), which are necessary to get the show on the road. Explanations that rely only on efficient causes may become overly mechanistic, thereby distracting investigation from the substrates, underlying mechanisms, and functional aspects.

Material causes (machinery) refer to the substrates, the underlying mechanisms. These causes are of most interest to medical and health professionals who are trained to understand, diagnose, and treat problems with underlying machinery. For instance, high blood glucose may be due to diabetes (formal cause) that may result from insufficient production of insulin (material cause), complicated by eating Twinkies (efficient cause). Parents often turn to material causes to explain challenging behavior in children, particularly when the efficient causes and triggers are inconspicuous and difficult to pin down accurately. “Lacks motivation” is too often the ad hoc explanation by family members; “Lacks character” by neighbors. Explanations that rely exclusively on material causes can become reductionistic, omitting relevant connections to triggers and consequences.

Final causes (functions) are the purposes of an event, what has brought about or sustained a phenomenon or process. Not all phenomena have final causes, or are directly understandable in terms of them. Cerebral edema, for example, is a rescue mechanism of the brain that in extreme can have serious negative consequences. Thus, some outcomes may represent break-down or failure modes of systems, some of which may serve an important function in normal circumstances. Proximate final causes may refer to the immediate consequences of some behaviors or misbehaviors, such as ones that may sometimes occur with the syndrome of TBI: escape and avoidance of difficult situations. Ultimate final causes may involve a learning history that has resulted in current maladaptive behavior.

PART TWO:  Applying Aristotle’s framework to neurobehavioral treatment and the role of Behavior Analysis

When a person becomes aggressive following a brain injury, we quickly try to comprehend the event. We start with a description such as: “He struck the therapist during his therapy session.” This triggers communication with the family, therapists and staff, the physician and other medical professionals, the case managers, insurance adjusters, and so on. The descriptions of the incident set each on their respective paths to explain behavior in order to derive an effective intervention. Agitation has crossed the formal threshold to aggression: physical or verbal behavior directed at another person with the intention to cause harm. We want to know about the specific necessary and sufficient conditions that triggered the aggression (efficient causes), underlying mechanisms (material causes), the function or purpose it served (final causes), and best ways to talk about it, both for treatment, and for communication with family members (formal causes). We may require details about immediate (proximate) variables, as well as enduring variables from the past (personal history, family history) suggesting ultimate reasons for such aggression. In short, we need to communicate much information in a brief period of time for intervention to commence, and we need to continue dialogue throughout treatment to be sure that the stakeholders share our framework.

A Case Study

Sam is a 50-year old male who received a significant brain injury when he was struck by a motor vehicle at the age of 14. Prior to admission to our facility, Sam spent most of his adult life residing at institutional settings where he exhibited physical and verbal aggression, requiring an increased level of staff supervision, and occasional temporary placement in isolated sections of the referring facility.

Upon admission to our program, a functional assessment of problem behaviors (Questions About Behavior Function – QABF) was conducted. The results suggested that physical and verbal aggression were functionally related to attention delivered by caregivers or therapists: When caregivers’ and therapists’ attention to Sam decreased, the probability that he would engage in physical and verbal aggression resulting in attention from others (e.g., redirection, physical intervention or containment) increased. He had the staff on a schedule of negative reinforcement: their lack of attention generated an increase in the frequency of aggression that resulted in a swift staff reaction to escape or delay his aggressive behavior.

On the basis of the functional assessment, differential reinforcement of alternative behavior (DRA) was introduced to treat aggression. Under this procedure all caregivers and therapists: (1) provided little or no attention upon physical and verbal aggression by Sam; and (2) shifted the schedule of reinforcement to deliver attention contingent upon Sam’s use of more cordial, alternative attention-requesting behaviors. During the course of treatment his antipsychotic medications were tapered and discontinued as aggressive behaviors decreased.

Figure 1 summarizes the medication adjustments for Sam during treatment. Data for verbal and physical aggression were recorded according to a 30-min partial interval count for occurrence/non-occurrence of target behaviors.

Vertical dashed lines indicate medication adjustments during the course of treatment, and labels indicate the name of the medication and the adjusted dose. Down-arrows preceding medication labels indicate reductions and discontinuations; up-arrows preceding medication labels indicate increases or initiations. From the slope of the curve we may infer changes in response rates— decreases in the slope of the curve over time (negative acceleration) indicate decreases in the occurrence of aggression. In general, these data show variable but negatively accelerating trends; physical aggression rates (dashed line) were lower than those for verbal aggression (continuous line).

Reductions in trazodone and risperidone often occasioned brief bursts of verbal aggression, which gradually decreased to low or zero rates until the next medication taper. Concurrent with the discontinuation of risperidone, Sam developed bursitis in his elbow from an infection that required medical attention. This brief delivery of attention was correlated with extreme verbal and physical aggression in response to pain in his elbow. After medical treatment was administered, DRA treatment was reinstated for the remainder of the study. However, it was unclear whether this brief delivery of medical attention inadvertently produced and sustained the higher rates of aggression that lasted for approximately five weeks, until risperidone was reinstated, producing a gradual reduction in the frequencies of target behaviors. When these target behaviors approached zero rates, clozapine was introduced and substituted for risperidone, producing brief but decreasing bursts of target behaviors. Subsequently, risperidone was discontinued without any increase in aggression, as was clozapine.

In this example the search for efficient causes (decrease in level of staff attention) and final causes (attention received) resulted in an intervention to change the triggers and consequences. Aggression gradually decreased as a function of shifting the contingencies of reinforcement. This functional relation was confirmed inadvertently when the brief, but intense complaints of pain by Sam produced an unavoidable medical attention to treat bursitis. Additionally, a material explanation (chemistry potentially more responsive to clozapine than to risperidone) produced an intervention based on a review of the current medications and a gradual taper to determine therapeutic effectiveness, and eventual substitution of medications that was either more effective or had fewer agitating side effects. This case history constitutes one more example of attempts at efficient and material explanations, inquiries that expose a range of variables with the potential to contribute to understanding complex behaviors ranging from ADHD (Killeen, Tannock,  & Sagvolden, 2012), to hypnosis (Killeen & Nash, 2003). 

Further benefits from analyses of efficient causes

Closer examination of subtle environmental triggers and contingencies reveals interesting and unexpected efficient causes for behavior that can inform neurobehavior treatment. Recent research, (Mace, McComas, Mauro, Progar, Taylor, Ervin, & Zangrillo, 2010), for example has suggested that DRA procedures may actually prolong extinction effects (causing “extinction bursts”) due to behavioral momentum, thereby prolonging the persistence of target behaviors. Conducting a DRA procedure in a separate context from which learning the target behavior occurred can, however, decrease resistance of the problematic behavior to extinction. Similarly, there are situations in which the extinction component of the DRA procedure cannot be implemented— combative behavior may be too intense to stop or directed toward others in ways that cannot be ignored. In a series of experiments Athens and Vollmer (2010) demonstrated that behavior treatment plans that involve manipulating reinforcer duration, quality, delay, or a combination of these in ways that favors appropriate behavior rather than problem behavior can still produce more appropriate responses, even though problem behavior received occasional (albeit, lower) reinforcement. In both of these cases, the procedures have some risks consequent on implementation (increases in target behavior), but these can be minimized with refinement of the consequences (final causes) thereby averting the need to use medications (material necessary causes) to address the problem.

Behavior analysis techniques can yield benefits in addition to merely addressing problem behaviors as in the above example. An analysis of triggers and consequences can produce more robust effects when teaching adaptive living skills. Decades of research in applied behavior analysis has generated instructional methods for teaching in homes and classrooms, as well as vocational and rehabilitation settings, such as errorless learning (Chandonnet & Kupfer, 2014; Sidman, 2012), fluency and precision teaching (Binder, 1996), and stimulus equivalence training (Sidman, 1994). Research suggests that efficient and final explanations are primarily useful when there is a problem behavior to reduce or eliminate, but other formal explanations (e.g., TBI patients often lack social competence) help clarify potential deficiencies in appropriate responding that may be the result of environmental contingencies that sustain inappropriate behaviors. Thus, if the individual with brain injury could acquire skills in PT, OT, SPL, and so on more quickly and effectively by changing teaching methods, problem behaviors might be less likely to occur. Teaching methods derived from ABA (efficient and final causes) thereby complement those methods used to increase brain, body, and sensory health (material causes).

A thorough bibliography of evidence-based teaching methods for persons with brain injury is located on the Brain Injury Webpage for the Cambridge Center for Behavioral Studies:

Pursuing interrelationship between efficient and material causes

            What are the interactions between efficient causes and material causes? In the example of the broken lamp, one family member focused on reckless behavior in the home, but another alluded to the causes involving the environment—a wobbly lamp, an accident waiting to happen. In neurobehavioral treatment, proximate (temporally immediate, relevant and conspicuous) influences over behavior are revealed during initial assessments and ongoing progress reviews, but access to past environmental events or historical influences (medical records, psycho-social histories, interviews, and verbal reports) are relevant as well. Expanding the causal time frame, an examination of family history may reveal generational patterns that implicate ultimate genetic influence. Neurobehavioral approaches do not simply treat a person with a brain injury; they provide treatment within a context of immediate and historical influences.

Figure 2 represents the broader influences of both ultimate variables (across large timeframes) and proximate variables (most recent or conspicuously present) in the Aristotle’s framework to explain the causes of ADHD (Killeen et al, 2012). In this figure, the inner set are proximate (molecular) causes and the outer set ultimate (molar) causes. Triggers of symptoms (states) are proximate efficient causes; triggers of the phenotype (traits) are ultimate efficient causes. Material causes comprise the hardware underlying the behavior (proximate, neurophysiology) and the syndrome it instances (ultimate, structural, or genetic). Recursive arrows show outcomes can modify the system to change the sensitivity to correlated stimuli and responses through shifts in attention, learning, and reframing of the situation.

Isolating interactions between efficient and material causes of behavior is often difficult; however, the topic is of paramount importance in behavior analysis, particularly in relation to interactions between: genes and environment (Suomi, 2002), consequences, genes and brain development (Schneider, 2012), unique conditioning histories and drug effects (Branch, 2006; Terrace, 1963), and behavioral and biological systems (Thompson, 2007). Accordingly, the language of the behavior analysis community continues shifting to accommodate the expansion of efficient and material explanations (Hineline, 1980; Hineline & Groeling, 2011). Skinner (1989) had pointed us in this direction:

“There are two unavoidable gaps in any behavioral account: one between the stimulating action of the environment and the response of the organism, and one between consequences and the resulting change in behavior. Only brain science can fill those gaps. In doing so it completes the account; it does not give a different account of the same thing. Human behavior will eventually be explained (as it can only be explained) by the cooperative action of ethology [which we place as ultimate mechanism, an evolved organism in its niche], brain science [proximate machinery], and behavior analysis [formal, efficient and final causes].” (p.18)


When caregivers and family members seek explanations about behavior changes observed in patients with brain injuries, there is a distinction between “what” is happening, “why” it is happening and “how” it is happening. Addressing the “what” question requires careful analyses to ensure that behavior is not mischaracterized—that it is not, for instance, within the normal range of human responses. If the behavior is categorizable, it is essential that all plausible categories of explanation have been considered. Inferences to material and final causes should be avoided in first-level formal descriptions. These actions all address formal causes. A reference to “why” may lead to consideration of “what was gained by it”, a question about goals and reinforcers. But it may also refer to instigating factors. Thus “why” questions are cues to discuss both the triggers for behavior (efficient causes) and sustaining reinforcers (final causes) It may also reveal a concern over “structure and under lying mechanisms” that govern the behavior (material causes).

Neurobehavioral treatment should attempt to address all of these perspectives. Addressing all four causes (Formal, Efficient, Material, and Final) at relevant levels—molar and molecular—can lead to more comprehensive and inclusive strategies, and a more convincing understanding of behavior for patients, their families, and clinicians.


Athens, E.S., Vollmer, T.R. An investigation of differential reinforcement of alternative behavior without extinction. J Appl Beh Analy 2010;43:569-589.

Binder, C. Behavioral fluency: Evolution of a new paradigm. Beh. Analy 1996;19:163-197.

Branch, M. How research in behavioral pharmacology informs behavioral science. J Exp Analy Beh 2006;85:407-423.

Chandonnet, N., Kupfer, J. Errorless learning in therapy. Poster presented at Brain Injury Summit: A Meeting of the Minds, 2015, January, Vail CO.

Hineline, P.H., Groeling, S.M. Behavior-analytic language and interventions for autism. In E.A. Mayville & J.A. Mulick (Eds.), Behavioral foundations of effective autism treatment. NY: Sloan Publishing, 2011.

Hineline, P.H. The language of behavior analysis: Its community, its function, and its limitations. Behaviorism1980;8:67-87.

Hocutt, M. Aristotle’s four becauses. Philosophy 1974;49:385-399.

Killeen, P.R. The four causes of behavior. Cur Directions in Psych Sci 2001;10:136-140.

Killeen, P.R., Nash, M. The four causes of hypnosis. Int J of Clinic and Exp Hypnosis 2003;51:195-231.

Killeen, P.R., Tannock, R., Sagvolden, T. The four causes of ADHD: A framework. 2012;In S.C. Stanford & R. Tannock (Eds.), Behavioral neuroscience of attention deficit disorder and its treatment. 2012;9:391-425, Berlin, Germany: Springer-Verlag.

Kupfer, J., Eastridge, D., Buzan, R.D., Castro, J. Using cumulative graphs to evaluate the effects of medication adjustments combined with extinction procedures to decrease aggression. Symposium entitled: Welcome Back, MY LOVELY! Cumulative graphs in the analysis of behavior. Presented at the 38thannual meeting of the Association for Behavior Analysis, 2012, May, Seattle, WA.

Mace, F.C., McComas, J.J., Mauro, B.C., Progar, P.R., Taylor, B., Ervin, R., Zangrillo, A.N. Differential reinforcement of alternative behavior increases resistance to extinction: Clinical demonstration, animal modeling, and clinical test of one solution. J Exp Analy Beh 2010; 93:349-367.

Schneider, S.M. The science of consequences: How they affect genes, change the brain, and impact our world. NY: Prometheus Books, 2012.

Sidman, M. Equivalence relations and behavior: A research story. Boston: Authors Cooperative, Inc., 1994.

Sidman, M. Errorless learning and programmed instruction: The myth of the learning curve. Euro J of Beh Analy.2010;11:167-180.

Skinner, B.F. The origin of cognitive thought, Am Psych1989;44:13-18.

Suomi, S.J. How gene-environment interactions can shape the development of socioemotional regulation in Rhesus monkeys. In B.S. Zuckerman, A.F. Zuckerman, & N.A. Fox (Eds.), Emotional regulation and developmental health: Infancy and early childhood. NJ: Johnson and Johnson Pediatric Institute, 2002.

Terrace, H. Errorless discrimination learning in the pigeon: Effects of Chlorpromazine and Imipramine. Science.1963;140:318-319.

Thompson, T. Relations among functional systems in behavior analysis. J Exp Analy Beh.2007;87:423-440.

Post navigation


via Featured Article: Comprehending Aggressive Behavior Following A Brain Injury: An Explanatory Framework for Neurobehavior | Brain Injury Professional

, , , ,

Leave a comment

[BLOG POST] Sleep Disorders After Brain Injury, PTSD, TBI

Why Do So Many Survivors Have Sleep Disorders After Brain Injury?

January 2018,  Written by Bill Herrin

Click Here to sign up to receive a BULLETIN monthly!!!

January’s Brain Injury Journey Bulletin dives into the new year with a topic that often keeps people up at night…sleep disorders after TBI.

Sleep. It can be elusive, and one of the most frustrating things to accomplish after brain injury – especially on a consistent basis. Quite often, sleep disorders can take hold after brain injury – and cause everything from anxiousness to feeling depressed, tired, irritable, and more. In this issue of the Brain Injury Journey Bulletin, we’re going to take a look at all the things that sleep can affect, and some ways to conquer a sleep disorder after TBI.

Tossing and Turning

When your quality of life is being affected by lack of sleep, the desperation of wanting to rest can actually hinder you from getting the rest you need. Here are some changes in sleep patterns after TBI that are quite common:

  • difficulty falling asleep easily
  • trouble staying asleep throughout the night
  • waking up very early in the morning and not falling back to sleep
  • falling asleep and awakening far later than desired
  • purposely staying up late at night to get things done

Examples are:

  • You get into bed around 10 but it takes you several hours to fall asleep.
  • You wake up frequently during the night for no major reason.
  • You wake up at 4 in the morning and cannot fall back to sleep.
  • You’re up late every night working on the computer and your partner keeps asking
    you to come to bed.

Sleep Disorders and Other Factors

There are lots of different sleep disorders, and they can involve many different parts of the brain. Here are some of the more well-known sleep disorders that people encounter: Insomnia, extreme drowsiness, altered sleep patterns and Narcolepsy. Other disorders that can directly contribute to lack of sleep are Restless Leg Syndrome, teeth grinding or clenching, involuntary movements of your arms/legs during sleep, sleepwalking, sleep apnea, etc. Other factors that can deprive you from sleep are pain, alcohol, caffeine and nicotine, depression…and naps. A poorly timed nap (late in the day) obviously can end up backfiring on you later that night! It’s best to limit the length of naps so they help you get through the day, but don’t keep you up at night.

When PTSD is involved, especially in military veterans, sleep disorders can disturb sleep to the point of a person dreading bedtime, and efforts to quiet the symptoms with drugs or alcohol can make symptoms worse in the long run. Hyper-alertness, flashbacks, or nightmares can play a big part in keeping PTSD survivors up at night.

Research has found that sleep disorders are 3 times more common in persons with TBI than the general population, that about 60% of TBI survivors have ongoing problems with sleeping, that women are more affected than men…and that aging increases the likelihood of sleep problems.

This group has been researching how people sleep, and they have collected some great information about how drug addiction and recovery can affect a person’s ability to have healthy, restorative sleep….along with addressing other sleep disorders. You can read the full guide at this link.

Better sleep?

Sleep, when achieved regularly, brings a bevy of positive side-effects, and is an essential component of mental and physical well-being. It can affect healing of the brain and body, improve short-term memory and attention, improvement of your mood, and it can even reduce physical pain. The main thing that sleep obviously provides is that you feel rested and more alert!

How You Sleep Also Matters

Being uncomfortable can affect your sleep more than you realize, too. Here’s a link to an article on that covers different sleep positions, and how they can help (or hinder) sleep, or even cause pain in your back, neck, etc.  Here’s the link.

Talk It Over With Your Doctor

There are plenty of over-the-counter and off-the-shelf medications specifically made to help you “catch some ZZZZZ’s” – but it’s very important that persons with brain injury talk to their doctor about the side effects of sleep medications before using any of them.

Brain injury presents a variety of issues that can cause stress, and the stress can easily parlay itself into loss of sleep. If loss of sleep is wearing you down, or slowing your recovery after TBI, you should speak with a physician right away. Once you seek medical advice, the doctor can help you discover the causes and effects of your sleep issues, and discuss all possibilities of easing the loss of sleep. From sleep labs to prescription medications, to discussing techniques for easing your mind before bedtime, your doctor will hopefully help you resolve the sleep deprivation to some degree.

Suggested Reading

The person you are with little or no sleep, versus the one you are when well rested can be like the difference in…well, like night and day! Tips for managing your sleep schedule, and how to improve it, are available in this easy-to-read tip card – available on our website. It’s titled “Sleep after brain injury”, and if you go to this link, you can get a free tip card and catalog.  Here’s the link. for the catalog & tip card. Here’s more info on the SLEEP tip card.

New Year, New Sleep Habits?

With a new year started, you can reference any issues imaginable that relate to PTSD, TBI, ABI, brain injury, concussion, and more, on Lash & Associates’ blog page. Specifically relating to the new year, realistic resolutions after TBI, here is a blog article by Donna O’Donnell Figurski that talks all about it. Here’s the link.

Knowing that stress and anxiety (after TBI) can take its toll, this blog post by Marilyn Lash and Taryn Stejskal, discusses managing stress, and the symptoms of stress that become evident when they’re taking their toll on your health and well-being. Here’s the link.

Blog Posts Galore On A Wide Range of TBI Issues

Feel free to keyword search our entire collection of blog posts, many written by well-known experts, clinicians in the field of brain injury, and also people who have survived brain injury, had family members that have a TBI, and much more. It’s a treasure trove of information that is available for FREE, 24/7/365. It’s all for you at this link!

Resolution of sleeping issues is a “2018 Resolution” for the new year that many have added to their lists to  achieve. We hope that you have a great new year, and that you rest assured…and sleep well!





via Sleep Disorders After Brain Injury, PTSD, TBI

, , ,

Leave a comment

[WEB SITE] 7 signs of executive dysfunction after brain injury

7 signs of executive dysfunction after brain injury Main ImageExecutive dysfunction‘ is not, perhaps, a particularly well known term, but the effects of brain injury that it covers are very common indeed. It is used to collectively describe impairment in the ‘executive functions’ – the key cognitiveemotional and behavioural skills that are used to navigate through life, especially when undertaking activities and interacting with others.

Although executive dysfunction is a common problem among many brain injury survivors, it is most commonly experienced following an injury to the frontal lobe.

The importance of executive functions is shown by the difficulties caused when they don’t work properly and someone has problems with executive dysfunction. Since the executive functions are involved in even the most routine activities, frontal injuries leading to executive dysfunction can lead to problems in many aspects of life.

Here we list the most common effects of executive dysfunction, with some examples of common issues that brain injury survivors can face:

Difficulties with motivation and organisation

  • Loss of ‘get up and go’, which can be mistaken for laziness
  • Problems with thinking ahead and carrying out the sequence of steps needed to complete a task

Rigid thinking

  • Difficulty in evaluating the result of actions and reduced ability to change behaviour or switch between tasks if needed

Poor problem solving

  • Finding it hard to anticipate consequences
  • Decreased ability to make accurate judgements or find solutions if things are going wrong


  • Acting too quickly and impulsively without fully thinking through the consequences, for example, spending more money than can be afforded

Mood disturbances

  • Difficulty in controlling emotions which may lead to outbursts of emotion such as anger or crying
  • Rapid mood changes may occur, for example, switching from happiness to sadness for no apparent reason

Difficulties in social situations

  • Reduced ability to engage in social interactions
  • Finding it hard to initiate, participate in, or pay attention to conversations
  • Poor judgement in social situations, which may lead to saying or doing inappropriate things

Memory/attention problems

  • Finding it harder to concentrate
  • Difficulty with learning new information
  • Decreased memory for past or current events, which may lead to disorientation

Find out more

If you or someone you care for is affected by executive dysfunction, it is important to seek support. Speak to your doctor about your symptoms, and ask about referral to specialist services such as counselling, neuropsychology and rehabilitation.

You can find out more and get tips and strategies to help manage your condition on our executive dysfunction after brain injury page.

Headway groups and branches can offer support in your area, and you can contact our helpline if you would like to talk things through.

via 7 signs of executive dysfunction after brain injury | Headway


Leave a comment

[WEB SITE] Finding Freedom after Brain Injury – TBI Survivor


Is a little freedom too much to ask?

Free from worry. Free from pain. Free from confusion. Free from doubt. Free from all the “little” nagging, ever present stuff   that can make life after TBI difficult.

We focus on repairing ourselves so we can get back what we lost, but really, what we are looking for in one word, is freedom.

Those Limits

Many of us feel held back by the limits our brain injury has imposed on us. Sometimes there are physical limitations. Many times we have cognitive limitations or feel the pressure of  financial, family or societal constraints; we have no money and we feel like outcasts.

When you put all these factors together, you come up with a life half lived. How do we make it a full, free life, full of moments of living without a care, soaring through life like an eagle?

As I said earlier, we don’t often think of our life after brain injury in terms of freedom. Rather we discuss it in terms of recovery, or getting our life back.

Well, freedom is not just about what we are able to do. It’s about who we are.

What is Freedom?

We want to break the bonds that bind us, but we are so focused on this thing the doctors call recovery, that sometimes we forget to live our lives; it’s almost as if we are marking time until we get back to where we want to be, and we don’t allow ourselves to live or be free.

We all have different opinions on what it means for us to feel free, really free after experiencing a brain injury. Maybe you are looking for the freedom you feel when you’re skiing through a layer of soft, fluffy powder.  Or perhaps you want to feel as though you are on the beach in the Caribbean with the surf crashing around you. It could be that freedom for you is simply being in control of your destiny.

So often, we feel trapped– trapped in our bodies, our heads or our circumstances, as we attempt to live our lives after brain injury. It’s almost as if there are these invisible straps holding us down, and we feel trapped by a condition that affects everything we do, say or think.

We desperately want to escape from this heavy, dark curtain that has fallen over us, but we don’t know how, except to faithfully follow the regimen our therapists and doctors have mapped out for us.

We may not realize it, but when everything we do is governed by a desire to recover, recover, recover, we are being c0ntrolled by our brain injury. Maybe there is a way to be thinking about how to live, live, live instead. Maybe we have to change our ideas of what it means to live, to be alive, and how we seek those things that make us feel free.

The Banshee War Cry

One of the best examples I can share of achieving true, momentary freedom, occurred about two months after I was discharged from the rehab. We had gotten about a foot of snow, and a friend and I went to a nearby hill to go tobogganing. I don’t have a clear memory of it, but I believe it was early evening.  The hill we were going to come down was short and steep, with a long run out.

We dragged the toboggan to the top of the hill, lay it down and got on.  I took a breath and then we pushed off. It was the first time since I had awoken from my coma that I felt alive; my senses bombarded me with stimulation. The wind blowing in my face. The powder snow spraying all around me. The speed. The smell of fresh snow, and everything around us completely still…except for us of course. We barreled down the hill.

Temporarily, anyway, I was free.

I had forgotten what freedom felt like. I wasn’t worried about crashing. I wasn’t worried about hitting my head. I didn’t care if I wiped out. It was just me, my friend, the snow and the toboggan.

Overcome with the feeling that I could do anything, I gave a loud “Whoop!”, like a war cry, when we were at our top speed.

I saw the importance of stringing the small moments together, of living for every moment and taking nourishment from them because they gave me freedom. They gave me life.

That’s what I want for myself. That’s what I want for all of us: to feel free with no worries. To feel what it is like to be alive and be full of possibilities.

Thanks, Jeff


via Finding Freedom after Brain Injury – TBI Survivor

, , , , , ,

Leave a comment

[ARTICLE] Effects of somatosensory electrical stimulation on motor function and cortical oscillations – Full Text



Few patients recover full hand dexterity after an acquired brain injury such as stroke. Repetitive somatosensory electrical stimulation (SES) is a promising method to promote recovery of hand function. However, studies using SES have largely focused on gross motor function; it remains unclear if it can modulate distal hand functions such as finger individuation.


The specific goal of this study was to monitor the effects of SES on individuation as well as on cortical oscillations measured using EEG, with the additional goal of identifying neurophysiological biomarkers.


Eight participants with a history of acquired brain injury and distal upper limb motor impairments received a single two-hour session of SES using transcutaneous electrical nerve stimulation. Pre- and post-intervention assessments consisted of the Action Research Arm Test (ARAT), finger fractionation, pinch force, and the modified Ashworth scale (MAS), along with resting-state EEG monitoring.


SES was associated with significant improvements in ARAT, MAS and finger fractionation. Moreover, SES was associated with a decrease in low frequency (0.9-4 Hz delta) ipsilesional parietomotor EEG power. Interestingly, changes in ipsilesional motor theta (4.8–7.9 Hz) and alpha (8.8–11.7 Hz) power were significantly correlated with finger fractionation improvements when using a multivariate model.


We show the positive effects of SES on finger individuation and identify cortical oscillations that may be important electrophysiological biomarkers of individual responsiveness to SES. These biomarkers can be potential targets when customizing SES parameters to individuals with hand dexterity deficits. Trial registration: NCT03176550; retrospectively registered.


Despite recent advances in rehabilitation, a substantial fraction of stroke patients continue to experience persistent upper-limb deficits [1]. At best, up to 1 out of 5 patients will recover full arm function, while 50% will not recover any functional use of the affected arm. [2] Improvement in upper limb function specifically depends on sensorimotor recovery of the paretic hand [3]. Yet, there remains a lack of effective therapies readily available to the patient with acquired brain injury for recovery of hand and finger function; a systematic review found that conventional repetitive task training may not be consistently effective for the upper extremity [4]. It is thus critical to explore inexpensive and scalable approaches to restore hand and finger dexterity, reduce disability and increase participation after stroke and other acquired brain injuries.

Sensory threshold somatosensory electrical stimulation (SES) is a promising therapeutic modality for targeting hand motor recovery [5]. It is known to be a powerful tool to focally modulate sensorimotor cortices in both healthy and chronic stroke participants [5678]. Devices such as transcutaneous nerve stimulation (TENS) units can deliver SES and are commercially available, inexpensive, low risk, and easily applied in the home setting [9]. Previous studies have demonstrated short-term and long-term improvements in hand function after SES [5101112131415]. However, the effect of SES on regaining the ability to selectively move a given digit independently from other digits (i.e. finger fractionation) has not been investigated. Poor finger individualization is an important therapeutic target because it is commonly present even after substantial recovery and may account for chronic hand dysfunction [16]. Further, it is unclear if SES is associated with compensatory or restorative mechanisms. Prior studies have largely relied on relatively subjective clinical evaluations of impairment, such as the Fugl-Meyer Assessment, or timed and task-based assessments, such as the Jebson-Taylor Hand Function Test. Biomechanical analyses, on the other hand, can provide important objective and quantitative evidence of improvement in neurologic function and normative motor control [1718]. Therefore, we aimed to determine not only the functional effects, but also the kinematic effects, of SES on chronic hand dysfunction.

Simultaneously, it should be noted that although SES can potentially be an effective therapy, not all individuals who are administered SES experience positive effects. While improvement levels as high as 31–36% compared to baseline function have been reported, [1119] about half of one cohort demonstrated minimal or no motor performance improvement after a single session of SES [15]. One method to shed more light on this discrepancy is to identify neurophysiological biomarkers associated with motor responses to SES. Neurophysiological biomarkers are increasingly used to predict treatment effects [2021]. Although some studies have examined biomarkers associated with treatment-induced motor recovery, to our knowledge none have been performed for SES [2223]. A recent study using electroencephalography (EEG) found that changes in patterns of connectivity predicted motor recovery after stroke [24]. At present, little is known about the effect of peripheral neuromodulation on EEG activity, how existing neural dynamics interacts with peripheral stimulation, and whether this interaction is associated with improvements in motor function. Associating EEG activity with treatment response may also provide mechanistic insight regarding the effects of SES on neural plasticity. EEG activity can also potentially be used as a cost-effective real-time metric of the time-varying efficacy of SES. This novel application of EEG information may help tailor treatment efforts while reducing the variability in outcome.

The main goal of this pilot study was to evaluate both changes in finger fractionation in response to SES and identify the associated neural biomarkers through analyses of EEG dynamics. Outcomes from this study have potential in designing targeted SES therapy based on neural biomarkers to modulate and improve hand function after acquired brain injury such as stroke (e.g. enrollment in long-term studies of the efficacy of SES).


Continue —>  Effects of somatosensory electrical stimulation on motor function and cortical oscillations | Journal of NeuroEngineering and Rehabilitation | Full Text

Fig. 1a Schematic representation of the method used for calculating the FCI. The participant is instructed to flex only the index finger as much as possible without flexing the other digits. b FCI is defined mathematically as the angle traversed by the middle finger (digit A) divided by the angle tranversed by the index finger (digit B) relative to the horizontal starting position. c Statistically significant change in mean fractionation from baseline to immediately after peripheral nerve stimulation. Fractionation improvement is indicated by a decrease in finger coupling index (FCI)


, , , , , , , , , , ,

Leave a comment

[WEB SITE] Drinking Alcohol After Brain Injury

Holidays are often a time of parties with alcohol. For many, it’s the season to celebrate with alcohol, to party with the holidays coming! How often have you heard that line – or is it an excuse? But you may have also heard comments from friends and family such as,

“You get angry when you drink.”

“I don’t like how you act when you’ve been drinking.”

“You turn into a different person when you drink.”

Or simply…

“Please don’t drink.”

Drinking alcohol after a brain injury – whether it’s beer, wine, mixed drinks, or hard liquor – often raises questions, comments or accusations along the lines of “Is that wise?” or “Should you be doing that?”

Responses often made are, “It’s calms my nerves.” Or “It helps me fall asleep.” Or It’s not a problem for me.” Or “Don’t make such a big deal out of it.” Or “I can handle it.” Sound familiar?

Talking about alcohol is too often a “hot” topic leading to arguments with name calling and accusations on one side that are met with denials and resistance by the other person. The choice may turn into arguing about it or avoiding talking about it.  Neither approach helps. Statistics tell the real story.

• Up to 2/3 of people with TBI have a history of alcohol abuse or risky drinking. Injuries can occur when people drink too much alcohol.

• Between 1/3 to ½ of people with TBI were injured while drunk.

• After a TBI, about half of survivors stop drinking or cut way back.

There are consequences for survivors – and for their families. Research finds that after a brain injury, drinking alcohol:

• Reduces brain injury recovery
• Increases changes of re-injury
• Magnifies cognitive impairments, and
• Puts the person at risk for emotional problems such as depression.
• For these reasons, abstinence or not drinking, is recommend or, “No use is the best use.”
Not drinking is one way to give the brain a chance to heal.

Alcohol and brain injury can have wide ranging effects including:
• A traumatic brain injury increases the risk for developing seizures.
• Alcohol lowers the seizure threshold and may trigger seizures.
• Not drinking can reduce the risk of developing post-traumatic seizures.

Another Brain Injury
• TBI survivors are 3 to 8 times at higher risk for another brain injury.

Mental Functioning
• Affects memory, mental speed, balance, and thinking.
• May affect survivors more than it did before their injury.
• Magnifies negative effects of brain injury.
• Can have negative mental effects over days to weeks even after drinking stops.

• Is a depressant.
• Increases risks of depression after brain injury.
• Reduces effectiveness of anti-depressant medications.

• Reduces testosterone production in men.
• Reduces sexual desire in men and women.
• Reduces sexual performance in men.
• Reduces sexual satisfaction in both men and women.

As if all this isn’t enough, consider the potential interaction between alcohol and other drugs and prescription meds.

Don’t mix alcohol and meds.

• Can diminish or multiply effects of some medications, increasing risks of overdose and death.

We can only give you the facts and information about alcohol and brain injury. The choice is yours.

To see this newsletter on our blog page, just CLICK HERE!

This newsletter features excerpts by Dr. Charles Bombardier from the chapter on “Alcohol and Other Drug Use after Brain Injury.”  If you’d like to explore this topic more, you will find it in the workbook:  Living Life Fully after Brain Injury

Sign up to receive the Brain Injury Journey Bulletin via email every month – it’s free, and you can share this link with your friends, too! Just click the link below to receive the bulletin in your inbox each month!

Sign up to receive a free catalog, along with a Tip Card of your choice!
For a wide array of blog articles/posts, please check out all of our subject categories. Click this link to see all of our blogs!

You’ll find our monthly specials HERE!  Follow the link for big savings on these Lash products!

This Brain Injury Journey Bulletin is intended to offer encouragement and support for TBI Survivors and Caregivers, Clinicians, Friends and Family, and more! We hope that you find it informative and helpful.

-Your friends at Lash & Associates Publishing   #LAPUBLISHING  

via Brain Injury Journey Bulletin for November!

, ,

Leave a comment

%d bloggers like this: