Posts Tagged Traumatic Brain Injury

[NEWS] Finding innovative treatments to help patients with traumatic brain injury

To treat a traumatic brain injury, researchers are thinking outside the box.

A traumatic brain injury can range from mild to severe, but is usually caused by a harsh bump or blow to the head. A patient may experience a moment of dysfunction on the mild end, to unconsciousness and loss in brain function on the severe end of injury.”

Kevin Ward, M.D., a professor of emergency medicine and biomedical engineering at Michigan Medicine and director of the Michigan Center for Integrative Research in Critical Care (MCIRCC)

According to the Centers for Disease Control and Prevention, TBI is a serious public health problem in the United States. In 2014, there were approximately 2.87 million TBI-related emergency department visits, hospitalizations and deaths throughout the nation.

“Unfortunately, the current diagnosis, monitoring and treatment strategies for TBI have not significantly progressed over the last 30 years and have been ineffective at reducing the extent of the injury,” Ward says.

Massey TBI Grand Challenge

Thanks to funding from the Joyce and Don Massey Family Foundation, MCIRCC hopes to improve treatment and survival rates for patients that experience a TBI. The Massey family had their own experience with TBI after a car accident injured mother and wife, Joyce Massey.

“Funding from the Massey Family Foundation has allowed us to institute the Massey TBI Grand Challenge,” Ward says.

“The Grand Challenge aims to bring interdisciplinary teams together to create high-risk, high-impact, milestone-driven solutions that address the golden hours of care, or the treatment administered during the initial hours after injury, plus the 24 to 48 hours of care after a severe traumatic brain injury.”

The funding also allows MCIRCC to host the Joyce Massey TBI Summit each fall. The conference brings together the nation’s leading experts and researchers to discuss the most pressing challenges facing TBI care and how to work together to find innovative solutions.

The Massey TBI Grand Challenge encourages researchers to come up with “innovative and disruptive” TBI solutions and pitch them to an independent panel of clinicians, innovation and commercialization experts, national TBI experts and Department of Defense representatives.

“All of these great minds come together to push past the borders of typical TBI care,” Ward says. “What starts as an idea, evolves and starts to take shape. Then the team participates in our Wolverine Den, or a U-M version of Shark Tank,pitching day with research behind their idea and support that it should be funded, as it could help potentially guide future treatments.”

Five projects were selected for funding this year:

Using light wavelengths to target cells

Thomas Sanderson, Ph.D., an associate professor of emergency medicine and molecular and integrative physiology at Michigan Medicine, says that while the molecular events happening in the body during a TBI are complex and can vary, mitochondria, or the organelles in cells that help them stay energized, appear to be a common contributor to brain injury.

The research team proposed a non-invasive therapy that uses light wavelengths to target mitochondria and alter the molecular events happening inside cells during a brain injury.

Project and researcher: Evaluating Non-Invasive Mitochondrial Modulation in a Translational Model of TBI; Thomas Sanderson, Ph.D.

Valproic acid in TBI patients

Valproic acid is a type of medication generally used to treat patients with epilepsy and psychiatric disorders. Now, researchers hope it could be used to treat TBI.

The funded project will further investigate if valproic acid can successfully be used to treat patients with TBI and if so, the funds will help support an Investigational New Drug application.

Project and researchers: Valproic Acid Treatment for Varying Severities of Traumatic Brain Injury; Ben Biesterveld, M.D., Hasan Alam, M.D., Manjunath Pai, PharmD, Jason Fawley, M.D., Aaron Williams, M.D., George Velmahos, M.D., Martin Sillesen, M.D., Glenn Wakam, M.D., and Michael Kemp, M.D.

Point-of-care device to monitor and measure biomarkers in real-time

Cerebrospinal fluid, the fluid found in the brain and spinal cord that protects them from trauma, and blood contain biomarkers that researchers say could play a role in how a TBI is diagnosed and monitoring the progression of the injury.

Mark Burns, Ph.D., and Frederick Korley, M.D., Ph.D., proposed a portable, point-of-care device that could measure biomarkers in the fluid and blood and display the results on a handheld device, such as a smartphone, within 15 minutes.

Project and researchers: Device for High Frequency and Real-Time Measurement of Biofluid Biomarkers; Mark Burns, Ph.D., Frederick Korley, M.D., Ph.D.

Intranasal insulin therapy to protect the brain

Intranasal insulin, or insulin nasal spray, is already in clinical trials for Alzheimer’s disease and stroke, but researchers hope to prove it can successfully protect the brain when a high-dose is given to a TBI patient soon after injury.

The nasal spray speeds up the ability for the hormone to get to the brain through small blood vessels in the nose, instead of waiting for it to enter and go through the bloodstream when administered in the arm or stomach.

The research team will study the neuroprotective effects of an early dose and a treatment strategy where non-medical providers could administer the dose to a TBI patient right after the injury takes place.

Project and researcher: Neuroprotection with Intranasal Insulin after Traumatic Brain Injury; Tulasi Ram Jinka, DVM, Ph.D., and Robert Neumar, M.D., Ph.D.

Device to measure and monitor systolic blood pressure

Systolic blood pressure indicates the amount of pressure in the arteries when the heart pushes blood through the arteries to the rest of the body. A drop of systolic blood pressure below certain levels can dramatically worsen TBI. Unfortunately, monitoring critical levels of systolic blood pressure is very difficult.

The research team previously developed a device that provides automated, targeted systolic blood pressure monitoring. In this project, the group will refine and test the next iteration of their device to ensure it can provide continuous readings of a patient with TBI’s systolic blood pressure and keep it at a level needed for optimal TBI management.

Project and researchers: STAT: Systolic Target Assessment Tool; David Hackenson, M.D., Hakam Tiba, M.D., and Kevin Ward, M.D.

Future care

MCIRCC encourages researchers, clinicians and stakeholders to attend its future TBI events.

“By working collaboratively, we can pioneer a new path to transform TBI care,” Ward says.

“We hope the innovations our MCIRCC members are researching now, will result in improved care in the near future.”

 

via Finding innovative treatments to help patients with traumatic brain injury

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[BLOG POST] Me, Myself, and My (More or Less) Creative I (after traumatic brain injury)

By Bill Herrin

Working with the topic of brain injury at Lash & Associates Publishing, I’ve heard on quite a few occasions that TBI can seriously alter a person’s ability to do certain things that they were once highly skilled at. Some basic things can also be affected, like driving a car, riding a bicycle, outdoor activities, walking/balance and more.

Many may also sustain a brain injury that affects them on an even deeper level – such as paralysis, cognition, thought patterns, speech, logic, etc. The one thing that is very intriguing about TBI is how it can affect creativity – and how it may change a more logical “left-brained” person, and make them more creative, imaginative, musical, or artistic. This also could bring the opposite effect to a more “right-brained” person and erase most or all of their previous creative strengths and talents. Although I’m not a TBI Survivor, I truly empathize with those who have dealt with these extreme changes and thought that it would be an interesting topic to explore.

One such case was Hilary Zayed. She worked as a teacher, was a flutist, a passionate horseback rider, and a mother of 2 grown children when she had a brain injury. Her recovery and subsequent reinvention of her prior life came with much hard work. She couldn’t enjoy music like she used to, so she worked toward finding a creative outlet – and soon discovered the art of making mosaics, paintings, and more.

After three years of being at home with a rotation of visiting nurses – often lying on the couch, she started to maneuver down the stairs to her art studio/space more and more. Some health professionals encouraged her to exhibit her works (art and writing), and soon she found herself doing several other solo shows across the Northeast. She found that sharing her experience through her art opened doors for others to be inspired to try harder after their own TBI. Here is a quote taken directly from Hilary’s book titled: Reinventing Oneself After Loss:

“One of the biggest lessons I learned was the importance of sharing my experience. It seemed to speak to people and inspire them to do the same. It felt as if the “butterfly effect” was happening and I was the one with the moving wings. As I finish writing this personal journey it has been almost seven years. I cannot say that I have fully reinvented myself but I have attempted to stay on course, refine my goals and continue to work hard on moving through

obstacles and leaning forward. Oddly, it was leaning forward on my horse, that fateful day, which changed my life. That action gave me the gift of making art and writing about it, on this journey to reinvent myself after loss.

May you find the courage to move forward as you deal with loss.”*

With every instance of people that make gains creatively after TBI, there are also people who suffer losses in the same arena. Being creative, artistic, musical, inventor, a writer, etc. is a gift that can be rewarding, and even help a person identify with others on a huge level. Losing that creative spark can be a harsh reality. Overall “loss of self” is basically the same thing, but it’s a huge transition for a creative person.

Shown below, I’m referencing an incredible article (by Dahlia W. Zaidel) that discusses the neurological changes that can take place in the brain of a creative person after a TBI, and also changes in a less creative person…here’s an excerpt:
“Neurological cases of visual artists who had practiced their craft professionally prior to the brain damage can help point the way to neuroanatomical and neurofunctional underpinnings of creativity. Approximately 50 or so cases with unilateral brain damage (largely in one side of the brain, and where the etiology is commonly stroke or tumor) have by now been described in the neurological literature (Rose, 2004Bogousslavsky and Boller, 2005Zaidel, 20052013a,cFinger et al., 2013Mazzucchi et al., 2013Piechowski-Jozwiak and Bogousslavsky, 2013).

The key questions concern post-damage alterations in creativity, as well as loss of talent, or skill. A review of the majority of these neurological cases suggests that, on the whole, they go on producing art, sometimes prolifically, despite the damage’s laterality or localization (Zaidel, 2005). Importantly, post-damage output has revealed that their creativity does not increase, nor diminish (Zaidel, 200520102013b). Given that the damage arises unilaterally (only one or the other hemisphere), artistic creativity in the healthy brain can not simply be attributed to a single hemisphere, dedicated neural “regional center”, network, or pathway, but rather to a diffusely represented capacity in the brain. Indeed, it would further seem that creativity is highly sensitive to brain damage, more so than artistic productivity, talent, or skill.

We could speculate that in the healthy brain cognitive associative networks in the left hemisphere alone, in the right hemisphere alone, or both hemispheres working together contribute to the creative process in art. However, recent functional neuroimaging evidence based on non-artistic behavior in healthy volunteers points to greater left hemisphere involvement in creativity (Gonen-Yaacovi et al., 2013). Where do the original ideas in the artwork arise, is a complex question that researchers would like understand (Dietrich and Kanso, 2010Heilman and Acosta, 2013Jung and Haier, 2013). The likely answer with regards to the cerebral hemispheres is that both are functional in exceptional creativity, but with each hemisphere contributing a different facet, yet little understood, to the creativity process (Zaidel, 2013d).”**

From the most basic approaches to eye/hand coordination, thought and cognition, and creative expression – to advanced creativity and artistic endeavors after TBI, the persistence and determination required to persevere takes incredible inner strength. As I often say, every person’s TBI is different, and each has its own starting point – and the ending point remains to be determined. Finding your way through the maze of TBI (of which there may be many causes such as concussions, blast injuries, stroke, etc.) is one of total commitment to stay the course. Time, along with effort brings results for many TBI survivors, but not all.

It’s my hope to encourage you in your creative outlets, to find solace in your “new normal”, and to express yourself through creativity…and creativity doesn’t just have to be visual arts, it can be writing, crafting, music, knitting or crocheting, poetry, relaxing with an adult coloring book, and lots more. Everything we see around us was created by someone – including the devices we are reading this post on! Make the most of every day, and my prayer for all of us is that we find abundant personal reward from all that we aspire to accomplish in life…creative or otherwise!

Feel free to leave a comment, and share your story regarding the changes in creativity, too. It may inspire, it may not…but your story is important – and it’s worth sharing!

**Here is the link to the entire referenced article by Dahlia W. Zaidel:

https://www.frontiersin.org/articles/10.3389/fnhum.2014.00389/full

via Me, Myself, and My (More or Less) Creative I (after traumatic brain injury)

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[Abstract] Cognitive Training in Young Patients With Traumatic Brain Injury: A Fixel-Based Analysis

Background. Traumatic brain injury (TBI) is associated with altered white matter organization and impaired cognitive functioning.

Objective. We aimed to investigate changes in white matter and cognitive functioning following computerized cognitive training.

Methods. Sixteen adolescents with moderate-to-severe TBI (age 15.6 ± 1.8 years, 1.2-4.6 years postinjury) completed the 8-week BrainGames program and diffusion weighted imaging (DWI) and cognitive assessment at time point 1 (before training) and time point 2 (after training). Sixteen healthy controls (HC) (age 15.6 ± 1.8 years) completed DWI assessment at time point 1 and cognitive assessment at time point 1 and 2. Fixel-based analyses were used to examine fractional anisotropy (FA), mean diffusivity (MD), and fiber cross-section (FC) on a whole brain level and in tracts of interest.

Results. Patients with TBI showed cognitive impairments and extensive areas with decreased FA and increased MD together with an increase in FC in the body of the corpus callosum and left superior longitudinal fasciculus (SLF) at time point 1. Patients improved significantly on the inhibition measure at time point 2, whereas the HC group remained unchanged. No training-induced changes were observed on the group level in diffusion metrics. Exploratory correlations were found between improvements on verbal working memory and reduced MD of the left SLF and between increased performance on an information processing speed task and increased FA of the right precentral gyrus.

Conclusions. Results are indicative of positive effects of BrainGames on cognitive functioning and provide preliminary evidence for neuroplasticity associated with cognitive improvements following cognitive intervention in TBI.

via Cognitive Training in Young Patients With Traumatic Brain Injury: A Fixel-Based Analysis – Helena Verhelst, Diana Giraldo, Catharine Vander Linden, Guy Vingerhoets, Ben Jeurissen, Karen Caeyenberghs,

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[WEB SITE] Marijuana could be effective against traumatic brain injury

Although the lives of patients dealing with a traumatic brain injury have improved manifold in recent years, they find themselves vulnerable to a host of side-effects that come with the modern-day medicine such as opioid painkillers, antidepressants, mood stabilizers and anti-seizure medicines.

The good news, however, is that we can now make use of legal cannabis to treat a traumatic brain injury, without the fear of death and other side-effects (recall, marijuana consumption has never resulted in a single death thus far).

A study published in 2014 found that testing positive for THC while sustaining a traumatic brain injury was associated with decreased mortality – from 11.5% to down to just 2.4%. In this post, we’ll take a look at the available research and scientific evidence that may help us determine if (and how) marijuana could help improve the condition of a person battling TBI.

Symptoms of a traumatic brain injury

TBIs occur because of a severe blow to the head, typically during an athletic event or a road accident. The common symptoms include:

  • Mood swings
  • Headaches
  • Seizures
  • Difficulties while speaking
  • Loss of motor control
  • Loss of memory

How cannabis could prove to be a breakthrough

1) Relieving Symptoms

Cannabis-derived medicines are known to drastically reduce the intensity and frequency of some types of seizures, while at the same time also displaying potent anti-anxiety and antidepressant effects, and that too without any serious side-effects.

Interestingly, a 2017 survey of 271 medical marijuana patients found that nearly 63% of participants preferred cannabis over prescription medications for the management of pain and anxiety.

2) Protection against a TBI

In order to understand this point well, you first need to have a clear understanding of the term ‘endocannabinoids’. Just like a cannabis plant produces phytocannabinoids (CBD, THC), the human body naturally produces similar molecules named endocannabinoids, which are used by the nervous and immune system to communicate.

A number of pre-clinical studies like this have shown that endocannabinoids have neuroprotective properties, which helps the brain and nervous system to recover after a blow.

It has been seen in animal models that CBD works by boosting levels of the body’s own endocannabinoids; while THC — the compound responsible for the “high” — works by taking the place of natural endocannabinoids itself in the body.

Growth of new brain cells

A study from the University of Saskatchewan (2005) found that when rodents were administered with synthetic THC, the cannabinoid apparently boosted the growth of new brain cells in a region known as the hippocampus.

The hippocampus region is responsible for memory, learning and the autonomic nervous system; research has shown that patients battling anxiety and depression often have this portion of their brain adversely affected.

Hence, the growth of new cells, courtesy of cannabis, may help in tackling the situation.

Reduced Brain inflammation

It is a well-known fact that CBD has anti-inflammatory properties. Preclinical research has found that CBD treatment immediately after a loss of oxygen can significantly reduce brain damage.

This 2011 study found that CBD treatment administered to newborn pigs after an injury effectively reduced brain edema, seizures and improved overall motor skills and behavior within just 72 hours after the injury.

Conclusion

The power of cannabinoids should never be underestimated. It’s only a matter of time before cannabis replaces most of the opioid medicines in use for traumatic brain injury treatment.

 

via Marijuana could be effective against traumatic brain injury

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[ARTICLE] Pharmacological management of long-term aggression secondary to traumatic brain injuries

Abstract
Aggression is common after traumatic brain injuries (TBI) in acute and chronic settings. However, there is limited guidance regarding its assessment and effective management. Whilst a number of pharmacological options are available for long term treatment, the evidence base is not of an adequate strength to support a unified practice. This article will explore the currently available guidelines and recommendations for treating chronic aggression after TBIs and evaluate the evidence for its pharmacological management.


Introduction

Aggression is a long term neurobehavioural sequelae of TBIs with incidences quoted from 11.5-33.7%.1 In TBI patients, aggressive behaviour tends to be impulsive rather than premeditated and can manifest as episodic dyscontrol syndrome, disinhibition or exacerbated premorbid antisocial traits.2 The underlying mechanisms of aggression are complex allowing numerous and diverse interventions targeting various pathways.

In acute settings, Lombard and Zafonte (2005) describe non-pharmacological measures to manage aggression including environmental alterations and ensuring minimal or non-contact restraints. Screening for systemic causes, optimising pain control and patients’ sleep-wake cycle are also advocated. In the event of failed non-pharmacological treatment, Lombard and Zafonte (2005) recommend that medication choice should be tailored to individuals; with side effect profiles taken into consideration.3

For chronic aggression, psychological therapies are used as a first line with pharmacological interventions trialled in later stages.4 Psychological therapy options include cognitive behavioural therapy (CBT), behavioural management utilising operant learning theory and contingency management. However, a review by Alderman (2013) concluded that further evidence using scientific methods is needed to analyse these approaches.5  Comparatively, there is a diverse body of literature addressing long term pharmacological treatment although quality among studies are varied. This article will focus on the aetiology for chronic post TBI aggression, current management guidelines and the evidence for long term pharmacological interventions.

Aetiology

Post TBI aggression has been associated with lesions affecting the prefrontal cortex – particularly the orbitofrontal and ventromedial areas – causing a loss of behavioural regulation. Disruption to inhibitory pathways between the prefrontal cortex and limbic system also results in limbic kindling and inappropriate emotional responses to negative stimuli thus facilitating aggressive behaviour.2 Associated neurotransmitter abnormalities include low cortical serotonin and impaired gamma amino-butyric acid (GABA)/ glutamate levels.6 Altered catecholamine and cholinergic levels are associated with cognitive impairment2 thus distorting information processing and predisposing patients to aggression.6 In TBI patients, underlying anxiety, affective disorders, seizures and frontal lobe dysfunction also increase susceptibility.10

Differentials for aggression

When identifying a cause for chronic aggressive behaviour, a patient’s previous experiences, comorbid psychiatric conditions and alcohol and/or substance abuse must be established with a collateral history.2,7  McAllister (2008) highlights the importance of determining pre-injury behaviour in order to exclude the possibility of symptoms being an exaggeration of pre-injury personality traits.8 Additionally, psychosocial factors must be deduced to identify possible triggers.2,7

Clinicians must be aware that aggression can be a presenting feature of other psychiatric disorders. Depression has a prevalence of 18.5% to 61% in post-TBI patients  and is linked with aggression due to their shared association with frontal lobe lesions and serotonin level imbalance.9 Other differentials include manic disorders (which can involve a more marked aggressive component if secondary to TBIs), anxiety disorders and alcohol and/or substance abuse. Personality and behavioural disorders such as affective lability, behavioural disinhibition and acquired antisocial behaviour should also be considered.8

Management guidelines

The National Institute for Health and Care Excellence (NICE) refers to the Scottish Intercollegiate Guidelines Network (SIGN) for rehabilitating patients with acquired brain injuries (ABIs). Psychological treatments advocated by SIGN include CBT, contingency management procedures, music therapy and comprehensive neurobehavioural rehabilitation (CNR).10 Family involvement appears to be associated with better outcomes2 and is also recommended.10

Of the studies quoted by SIGN, CNR was found to cause a positive effect in ABI patients in one systematic review although inconsistent results were obtained for the other three methods. Regarding pharmacological treatment, SIGN advises propranolol and pindolol as first line options.10

Pharmacological treatment

The aberrant neurotransmitter changes in the cortex and limbic areas as a result of TBIs2 provide targets for pharmacological therapy (as summarised in Table 1). Theoretically, cortical behavioural regulation can be enhanced by serotonergic agents and antagonists of dopaminergic and noradrenergic neurotransmission. Limbic hyperactivity can be dampened by the use of gamma aminobutyric acid (GABA) agonists, glutamatergic antagonists and anticholinergics.6

Impaired behavioural regulation

Antidepressants

Selective serotonin reuptake inhibitors (SSRIs) are indicated for their increase in dopamine and serotonin availability and the treatment of depression contributing to aggressive behaviour. In a trial conducted by Kant et al (1998), sertraline reduced aggression within one week of treatment although TBI severities were variable within the population.11 These results are mirrored in other trials presenting sertraline as a viable treatment option.12 Citalopram used in conjunction with carbamazepine successfully treated behavioural symptoms in a clinical trial of 22 patients conducted by Perino et al (2001)13 although the separate effects of both drugs are impossible to differentiate. A case study by Sloan et al (1992) found that fluoxetine improved emotional lability in one patient within a week.13

Tricyclic antidepressants have been shown to be useful for managing both post-traumatic and chronic aggression. Amitriptyline has reduced aggression with good tolerability despite its strong anticholinergic side effects in several studies and is suggested as the best option for treating behavioural disorders secondary to frontal lobe injuries without impairing cognition.13

Antipsychotics

There is a wide body of literature advocating antipsychotics for managing aggression due to their sedative effects.13 Nevertheless, the cognitive and extrapyramidal side effects of typical antipsychotics limit their value for chronic use. Comparatively, atypical antipsychotics have a milder side effect profile and are preferred although their cognitive impact in TBI patients is unclear.2 Furthermore, unlike older generations, atypical antipsychotics antagonise 5HT2 receptors and are therefore implicated in reduced aggression.9

Of the typical antipsychotics, chlorpromazine reduced explosiveness in one case study conducted by Sandel et al (1993). Various case studies also report haloperidol improving chronic agitation in TBI patients although significant side effects were encountered.13 Of the atypical antipsychotics the level of evidence is low. Quetiapine reduced aggression and irritability in seven patients in a trial conducted by Kim and Bijlani (2006).11 Olanzapine significantly reduced aggression within six months in a case study conducted by Umansky and Geller (2000). Clozapine was associated with varying levels of improvement in six case studies conducted by Michals et al (1993) however seizures were experienced in two patients.13

Overall, there is no reliable evidence advocating antipsychotic use for managing chronic post-TBI aggression. If antipsychotics are commenced for this purpose, it is suggested that their use is restricted to patients with psychosis.13

Beta blockers

Beta blockers are useful for cases where aggression is caused by underlying anxiety13 due to its inhibition of noradrenergic levels.9 A Cochrane review of four RCTs found that pindolol and propranolol reduced aggression within two to six weeks of starting treatment in ABI patients however no recommendations were made due to heterogeneity between samples, a small number of trials and small sample sizes.  The authors acknowledge that the trials involved high doses and so recommend caution when prescribing beta blockers for aggression.4

Methylphenidate

Methylphenidate is a psychostimulant indicated for its enhancement of dopamine and noradrenaline in the frontal lobe improving arousal and alertness.13 Mooney (1993) found in a single RCT that methylphenidate significantly improved anger scores in TBI patients.4 However other studies have yielded mixed results12,13 and no firm conclusion can be made.

Amantadine

Amantadine increases dopamine availability and acts on glutamatergic pathways. An advantage of its use is its non-sedating qualities however there is contradicting evidence for its efficacy.13 An RCT conducted by Schneider (1999) found no significant improvement4 however the trial was limited by a small sample size and large heterogeneity. Interestingly, studies of a lower level of evidence demonstrate favourable results.13 Due to this variability, its efficacy is still in question.

Buspirone

Buspirone – a serotonergic agonist licensed for treating anxiety13 – has also reduced aggression in several case studies2,12,14 warranting further research. Its side effects are amenable for use in TBIs although one disadvantage is its delayed onset.13

Hyperactive limbic drive

Anticonvulsants

The mood stabilising effects of anticonvulsants are mediated through their enhancement of GABA transmission.2 Carbamazepine has been demonstrated in studies to be effective for managing acute and chronic post- TBI aggression.12,13 Its side effects include impaired balance, sedation13 and cognitive impairment particularly in brain injured patients2 due to their heightened sensitivity. In a trial conducted by Mattes (2005), Oxcarbazepine reduced impulsive aggression however the number of TBI participants in the sample was unclear. Nine of the 48 participants also dropped out due to adverse effects11 suggesting more research is needed into its tolerability in TBI patients. Valproate has also been demonstrated to effectively manage behavioural and affective disorders13 with a milder cognitive impact compared to carbamazepine.2 Regarding other anticonvulsants, the evidence is of a lower standard. Pachet et al (2003) found that lamotrigine reduced aggression with good tolerability in one case study.11 Topiramate has been demonstrated to effectively treat manic symptoms but due to its side effects of psychosis and cognitive impairment,2 may be inappropriate for TBI patients. Case reports reference lithium to reduce post – TBI agitation however it may be unsuitable as a first line option due to its neurotoxicity.13

Benzodiazepines

Benzodiazepines are indicated for their anticonvulsive, anti-anxiety and sedative qualities facilitated by stimulation of the GABA receptor.13 There is limited literature on their chronic use in TBI patients due to their side effects of agitation, cognitive impairment and tolerance2 thus they are recommended to be more appropriate for cases of acute agitation or anxiety.11

Conclusion

There are many challenges in assessing and managing chronic aggression due to its complex aetiology. Previous literature presents a selection of pharmacological options however, their effect on TBI patients has not been confirmed resulting in limited guidance. The heterogeneity between samples also renders it impossible to predict treatment outcomes in the TBI population warranting the need for low doses, slow titration and frequent monitoring.13 A six-week trial period is advised by Fleminger et al (2006) to ascertain effects of treatment before trialling a new medication.4 Patient and family education regarding realistic treatment outcomes and side effects of treatments is also necessary to ensure treatment compliance.2 In future, a clarification of the underlying neurochemical changes is needed to identify further treatment targets. Additional larger scale RCTs are also needed to guide decision making and predict treatment outcomes. Table 2 offers a practical guide on medication choice in relation to aggressive behaviour in ABI.

References

  1. Tateno A, Jorge RE, Robinson RG. Clinical correlates of aggressive behaviour after traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(2):155-60.
  2. Kim E. Agitation, aggression and disinhibition syndromes after traumatic brain injury. NeuroRehabilitation 2002;17:297-310.
  3. Lombard LA, Zafonte RD. Agitation after traumatic brain injury: considerations and treatment options. Am J Phys Med Rehabil. 2005;84(10):797-812.
  4. Fleminger S, Greenwood RJ, Oliver DL. Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database Syst Rev. 2006;18(4):CD003299.
  5. Alderman N, Knight C, Brooks J. Rehabilitation Approaches to the Management of Aggressive Behaviour Disorders after Acquired Brain Injury. Brain Impairment. 2013;14(1):5-20.
  6. Siever LJ. Neurobiology of Aggression and Violence. Am J Psychiatry. 2008;165(4):429-42.
  7. McAllister TW. Neurobehavioral sequelae of traumatic brain injury: evaluation and management. World Psychiatry. 2008;7(1):3-10.
  8. Schwarzbold M, Diaz A, Martins ET, Rufino A, Amante LN, Thais ME et al. Psychiatric disorders and traumatic brain injury. Neuropsychiatr Dis Treat. 2008;4(4):797-816.
  9. Coccaro EF, Siever LJ. Pathophysiology and treatment of aggression. In: Davis KL, Charney D, Coyle JT, Nemeroff C, editors. Neuropsychopharmacology: The Fifth Generation of Progress. 5th ed. Pennsylvania: Lipincott, Williams & Wilkins; 2002:1709-23.
  10. Scottish Intercollegiate Guidelines Network. Brain injury rehabilitation in adults. Edinburgh: SIGN; 2013. 68 p. Report no.:130.
  11. Luauté J, Plantier D, Wiart L, Tell L, the SOFMER group. Care management of the agitation or aggressiveness crisis in patients with TBI. Systematic review of the literature and practice recommendations. Ann Phys Rehabil Med 2016;59(1):58-67.
  12. Warden DL, Gordon B, McAllister TW, Silver JM, Barth JT, Bruns J, et al. Guidelines for the Pharmacological Treatment of Neurobehavioral Sequelae of Traumatic Brain Injury. J Neurotrauma 2006;23(10):1468-501.
  13. Levy M, Berson A, Cook T, Bollegala N, Seto E, Tursanski S, et al. Treatment of agitation following traumatic brain injury: A review of the literature. NeuroRehabilitation 2005;20(4):279-306.
  14. Chew E, Zafonte RD. Pharmacological management of neurobehavioral disorders following traumatic brain injury – a state-of-the-art review. J Rehabil Res Dev 2009;46(6):851-79.

Anum Bhatti is currently in her final year of training for her MBchB at Keele University. She is interested in pursuing psychiatry as a career choice.

 

Dr George El-Nimr, MBChB, MSc (Neuropsych), MRCPsych, MSc (Psych), MMedEd, is a Consultant Neuropsychiatrist and Academic Secretary of the Faculty of Neuropsychiatry at the Royal College of Psychiatrists.

 

Correspondence to: Dr El-Nimr, Consultant Neuropsychiatrist, Neuropsychiatry Services, Bennett Centre, Richmond Terrace, Shelton, Stoke-on-Trent ST1 4ND. Tel: 01782 441614
Conflict of interest statement: None declared
Provenance and peer review: Submitted and externally reviewed
Date first submitted: 18/4/18
Date submitted after peer review: 21/9/18
Acceptance date: 15/5/19
To cite: Bhatti A, El-Nimr G. 
ACNR 2019;18(4);15-17
Published online: 1/8/19

via Pharmacological management of long-term aggression secondary to traumatic brain injuries | ACNR | Online Neurology Journal

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[Abstract] Evidence-Based Cognitive Rehabilitation: Systematic Review of the Literature From 2009 Through 2014 – Archives of Physical Medicine and Rehabilitation

Η εικόνα ίσως περιέχει: κείμενο

Abstract

Objectives

To conduct an updated, systematic review of the clinical literature, classify studies based on the strength of research design, and derive consensual, evidence-based clinical recommendations for cognitive rehabilitation of people with traumatic brain injury (TBI) or stroke.

Data Sources

Online PubMed and print journal searches identified citations for 250 articles published from 2009 through 2014.

Study Selection

Selected for inclusion were 186 articles after initial screening. Fifty articles were initially excluded (24 focusing on patients without neurologic diagnoses, pediatric patients, or other patients with neurologic diagnoses, 10 noncognitive interventions, 13 descriptive protocols or studies, 3 nontreatment studies). Fifteen articles were excluded after complete review (1 other neurologic diagnosis, 2 nontreatment studies, 1 qualitative study, 4 descriptive articles, 7 secondary analyses). 121 studies were fully reviewed.

Data Extraction

Articles were reviewed by the Cognitive Rehabilitation Task Force (CRTF) members according to specific criteria for study design and quality, and classified as providing class I, class II, or class III evidence. Articles were assigned to 1 of 6 possible categories (based on interventions for attention, vision and neglect, language and communication skills, memory, executive function, or comprehensive-integrated interventions).

Data Synthesis

Of 121 studies, 41 were rated as class I, 3 as class Ia, 14 as class II, and 63 as class III. Recommendations were derived by CRTF consensus from the relative strengths of the evidence, based on the decision rules applied in prior reviews.

Conclusions

CRTF has now evaluated 491 articles (109 class I or Ia, 68 class II, and 314 class III) and makes 29 recommendations for evidence-based practice of cognitive rehabilitation (9 Practice Standards, 9 Practice Guidelines, 11 Practice Options). Evidence supports Practice Standards for (1) attention deficits after TBI or stroke; (2) visual scanning for neglect after right-hemisphere stroke; (3) compensatory strategies for mild memory deficits; (4) language deficits after left-hemisphere stroke; (5) social-communication deficits after TBI; (6) metacognitive strategy training for deficits in executive functioning; and (7) comprehensive-holistic neuropsychological rehabilitation to reduce cognitive and functional disability after TBI or stroke.

via Evidence-Based Cognitive Rehabilitation: Systematic Review of the Literature From 2009 Through 2014 – Archives of Physical Medicine and Rehabilitation

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[BLOG POST] 7 Common Behavioral Effects of Brain Injury and How to Deal With Them – Jumbledbrain

A brain injury can have various physical, cognitive, medical, emotional, and behavioral effects on head injury survivors. Of these changes, behavioral changes can be one of the most challenging for survivors to overcome to live happier and more independently. To help survivors with traumatic brain injury (TBI), families and caregivers should learn to understand their behavior and develop practical ways to address those challenges.

Why Does Brain Injury Affect Emotions?

Behavioral problems following TBI are often the result of damage to the frontal lobe, the area of the brain that controls “executive functions.” Executive functions refer to the set of skills a person uses to plan, create, evaluate, organize, evaluate, reason, communicate, and solve problems. These impairments have a significant impact on how a person behaves.

Common Behavioral Changes Experienced by TBI Survivors

Human behavior is complex and multi-faceted. This means it can be difficult to isolate which behavior is a result of TBI. A TBI patient’s behavior is, after all, influenced by many different factors, like the nature of the injury, their pre- and post-injury experience, their cognitive abilities, or the behavior of other people. But some of the most common behavior changes encountered by TBI survivors include:

1. Memory Problems

Most people diagnosed with a brain disorder may experience memory problems, but they are more common among TBI survivors as a result of an injury from the bony protrusions inside the skull. Typical situations include forgetting a person’s name, losing a train of thought, and difficulty learning new things.

2. Temper Outbursts

Family members of people with TBI often describe their loved one as someone with a quick temper. They may use bad language, throw objects, or slam doors. Drastic changes like the loss of independence and inability to follow a conversation, in particular, can make a person with TBI more prone to these temper outbursts.

3. Depression

Depression among people with TBI can arise because of the struggle to adjust to disabilities and the changes to one’s role in the family and society. Symptoms of depression include feelings of worthlessness, suicidal thoughts, changes in sleep and appetite, and withdrawal from peers.

4. Poor Concentration

TBI affects a person’s attention and concentration abilities, posing a challenge to work, study, and everyday living. Poor concentration manifests itself in difficulty multitasking, following conversations, and processing information. This happens when the lateral intraparietal cortex—the region of the brain responsible for controlling attention—suffers damage.

5. Self-Centered Attitude

It’s common for TBI survivors to show signs of egocentrism. In turn, this could hamper their ability to see things from another person’s point of view which severely impact their relationship with family members, especially if they used to be a caring person. And although it is often taken for granted, the ability to understand another’s perspective is a complex cognitive skill.

6. Aggressive Behavior

Aggressive behavior following a TBI is often impulsive. A person with TBI can easily grow agitated over trivial disagreements. Experts explain that aggression that happens directly after the TBI is the result of delirium and other post-injury medications. Aggression up to three months after TBI, on the other hand, happens as a result of depression, chronic pain, and post-traumatic stress disorder.

7. Lower Sex Drive

A decreased desire or interest in sex is more common among TBI survivors than heightened libido. Disinhibited sexual behavior can be a possible effect of poor awareness and impulsivity. Changes in sexual functioning following TBI can be due to hormonal changes, medication side effects, fatigue, and movement problems.

Coping with a Loved One with Head Injury

People with TBI showing signs of these behavior problems should be evaluated by a doctor so they can receive proper treatment. On top of medical intervention, friends and family of survivors should also actively participate in rehabilitation, recovery, and advocacy.

1. Set Realistic Expectations

Brain injury has lifelong effects. It pays to understand that a person with TBI might already be trying his or her best. Every member of the family can have different abilities, skills, comfort levels, and limitations, so set small goals and acknowledge that every day is an achievement.

2. Get Involved

Behavioral problems are often hard to deal with. But try to resist the temptation of avoiding difficult situations. People with TBI could end up feeling more confused and isolated if left alone. Instead, get involved and familiarize yourself with their day-to-day routine.

3. Encourage Independence

Learning how to comfort a loved one with TBI is a must. But tread carefully: there is a fine line between caring for people and smothering them with affection. Try to instill independence and study their behavior to know the right time to provide comfort.

4. Reinforce Positive Behavior

What used to come easy to a TBI survivor may now feel extremely difficult. Reinforce positive behavior by focusing on the patient’s strengths, rather than pointing fingers or directing behavior.

5. Rediscover Preferences

Stay alert and pay attention to the wants and needs of a person with TBI. Discover new ways they can engage in activities and establish a balance between easy and difficult tasks. And always encourage them to participate, instead of assuming that their injury makes them unable to.

6. Confide with Loved Ones

Honesty is the best policy, and confiding in friends and family members can help alleviate the burden. Enlisting others for support can provide a fresh perspective and make it easier to identify triggers and how to avoid them.

7. Bounce Back Quickly

Accept that encountering behavioral problems is a part of life. Avoid getting stuck by teaching

new skills while a person is upset. Bounce back quickly from these obstacles then revisit them again later since people aren’t receptive to learning new things when they’re upset.

Other articles you may like:

Have you or a brain injury survivor you know struggled with these behavioural issues? What advice would you give to others?


Today’s article is written by Hazel Ann Westco.

Hazel Ann Westco is a start-up freelance writer. She is interested in writing blogs and articles related to legal cases mainly in personal injury and employment.  Whenever she has free time she rides her bicycle or motorcycle for a road trip. You can follow her on Twitter using her handle @AnnWestco.

via Guest post: 7 Common Behavioral Effects of Brain Injury and How to Deal With Them | Jumbledbrain

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[Infographic] Traumatic Brain Injury

traumatic-brain-injury-infographic

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[Abstract] Prevalence of Medical and Psychiatric Comorbidities Following Traumatic Brain Injury

Abstract

Objective: To examine the prevalence of selected medical and psychiatric comorbidities that existed prior to or up to 10 years following traumatic brain injury (TBI) requiring acute rehabilitation.

Design: Retrospective cohort.

Setting: Six TBI Model Systems (TBIMS) centers.

Participants: In total, 404 participants in the TBIMS National Database who experienced TBI 10 years prior.

Interventions: Not applicable.

Main Outcome Measure: Self-reported medical and psychiatric comorbidities and the onset time of each endorsed comorbidity.

Results: At 10 years postinjury, the most common comorbidities developing postinjury, in order, were back pain, depression, hypertension, anxiety, fractures, high blood cholesterol, sleep disorders, panic attacks, osteoarthritis, and diabetes. Comparing those 50 years and older to those younger than 50 years, diabetes (odds ratio [OR] = 3.54; P = .0016), high blood cholesterol (OR = 2.04; P = .0092), osteoarthritis (OR = 2.02; P = .0454), and hypertension (OR = 1.84; P = .0175) were significantly more prevalent in the older cohort while panic attacks (OR = 0.33; P = .0022) were significantly more prevalent in the younger cohort. No significant differences in prevalence rates between the older and younger cohorts were found for back pain, depression, anxiety, fractures, or sleep disorders.

Conclusions: People with moderate-severe TBI experience other medical and mental health comorbidities during the long-term course of recovery and life after injury. The findings can inform further investigation into comorbidities associated with TBI and the role of medical care, surveillance, prevention, lifestyle, and healthy behaviors in potentially modifying their presence and/or prevalence over the life span.

 

via Prevalence of Medical and Psychiatric Comorbidities Followin… : The Journal of Head Trauma Rehabilitation

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[Guideline] TELE-REHABILITATION INTERVENTIONS GUIDELINE – PDF File

TRIUMPH TRAUMATIC BRAIN INJURY GUIDELINES 2019

Tele-Rehabilitation Interventions through University-based Medicine for Prevention and Health

Download PDF File

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