Posts Tagged Neurobehavioral

[WEB SITE] Neurobehavioral Challenges After Brain Injury

The effects of neurological damage from events like trauma and stroke can be devastating to the individual and those close to them. Brain injury can result in lifelong physical, cognitive, and behavioral changes. The impact of behavior changes can profoundly alter how the injured person functions day to day, even impeding rehabilitative goals and impacting the ability to live independently. Changes in personality and behavior following traumatic brain injury (TBI) often represent the most significant barrier to a successful outcome including reintegration into the community whether for basic daily tasks, work or recreational/social activities.

Common behavior issues following brain injury include behavioral excesses (occurring too much) such as irritability (e.g., poor tolerance, short temper) and aggression (e.g., hitting, grabbing, kicking), property destruction (e.g., striking furniture, throwing items) and inappropriate vocalizations (e.g., cursing, yelling, threats). Also presenting a concern are behavior deficits (do not occur enough) such as compliance with tasks (e.g., cooperation with requests), social skills (e.g., overfamiliar discussions, uncharacteristically rude remarks), initiation (e.g., knowing when to begin tasks) and the academic and return to work skills (e.g., being on time, following directions) to be successful. Some of the most difficult behaviors can be dangerous to the patient and others around them. Treating these dangerous and challenging behaviors, which may include physical aggression toward others, self-injurious behavior, sexual disinhibition, and escape or elopement, requires a treatment commitment across the continuum of care.

In the early, acute stages of recovery from brain injury, many of the behavioral complications demonstrated are considered to be a normal phase of recovery. When these behaviors continue beyond those early phases, however, and form on-going negative patterns of interaction with others, very specialized treatment is required.  These behaviors can be disturbing to families and staff, disruptive to therapy, and jeopardize patient safety. The future quality of life for the patient and their family depends on effective interventions, provided with a great deal of consistency and structure. Behavior analysts (professionals in Applied Behavior Analysis) add value to interdisciplinary rehabilitation teams by helping to develop both skill acquisition and behavior reduction programs throughout the patient’s recovery (i.e., acute, post-acute, long term care). Behavior analysts spend a great deal of time directly observing interactions, determining what may be motivating the difficult behaviors, and what responses may need to be strengthened and reinforced. The behavior analyst must then provide training to all those who may interact with the patient, including most importantly, the family. This skilled, specialized intervention establishes more effective and acceptable response patterns that allow the patient to have their needs met and be better understood without displaying problem behavior. The structured behavior plan can also help the patient develop positive, prosocial responses, and more efficient functional skills.

The effects of brain injury are highly individual, which then challenges the behavior analysts, family and others on the treatment team to continually evaluate the responses, goals, and outcomes throughout recovery (e.g., monitoring response to new medications).

Considering the risk to patients and families, the rising healthcare cost and the possibility of reduced services being available, a focus on efficient and effective interventions such as behavior analysis seems essential to a well-integrated, interdisciplinary rehabilitation treatment team. The quality of life for those affected by brain injury depends on having the opportunity to receive not just the standard rehabilitation one might get following knee surgery but rather specialized, experienced and effective treatment specifically designed to address the unique difficulties they face including difficult behavior.

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[WEB SITE] Traumatic Brain Injury Rehabilitation at Florida Institute for Neurologic Rehabilitation

A Specialized Approach to NeuroRehabilitation & Traumatic Brain Injury Rehabilitation

The Florida Institute for Neurologic Rehabilitation, (FINR) has developed a comprehensive brain injury rehabilitation continuum of care offering specialized inpatient evaluation and treatment for both children and adults. Through a pre-admission evaluation and medical records review, FINR develops individualized treatment programs. As a leader in traumatic brain injury rehabilitation (TBI)neurorehabilitation, and neuropsychiatric disorders, our continuum of care delivers clinically relevant and cost effective services with unparalleled continuity of care. The distinct programs in our continuum are designed for individuals with a wide range of complex medical, neurorehabilitation, neurobehavioral, and neuropsychiatric care needs.

Potential traumatic brain injury rehabilitation clients, family members, funders, referral sources, and other concerned parties are encouraged to tour our facilities in order to make informed placement decisions. If our team of expert staff can assist in scheduling a tour or providing educational resources and information, please give us a call at 1-888-TBI-FINR (888-824-3467).

 

 

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[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: www.behavior.org.

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)

Conclusion

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.

References

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.

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[ARTICLE] Pharmacological interventions for traumatic brain injury – Full Text 

Psychostimulants, antidepressants, and other agents may speed the recovery of patients suffering from the functional deficits that follow an insult to the brain.

Traumatic brain injury is common in North America and has dramatic and wide-ranging effects on survivors’ quality of life. Those who survive traumatic brain injury may experience anxiety, agitation, memory impairments, and behavioral changes. When managing the immediate and long-term consequences of such injuries, clinicians have many pharmacological options, including psychostimulants, antidepressants, antiparkinsonian agents, and anticonvulsants. These and other agents can play a role in managing the neuropsychiatric, neurocognitive, and neurobehavioral sequelae of injury to the brain.

Traumatic brain injury (TBI) is commonly defined as an insult to the brain from an external force that causes temporary or permanent impairment in functional, psychosocial, or physical abilities.1 It is a significant cause of morbidity and mortality, and the leading cause of death and disability among young adults.

Common causes of TBI include motor vehicle accidents, falls, sports injuries, and violence,[1] and it is recog­nized increasingly in war zone injury.[2] In the US, approximately 2 million people will sustain a TBI each year, one-quarter of whom will require hospitalization, leading to a conservative estimate of direct and indirect costs of $50 billion to $100 billion annually.[3]

With advances in the management of head trauma, an increasing number of patients are surviving with residual neurological impairments. A National Institute of Health panel estimates that 2.5 to 6.5 million Americans currently live with TBI-related disabilities.[4]

The effective treatment of TBI requires input from multiple disciplines and professions starting at the time of injury and continuing through the rehabilitation phase.

Despite the prevalence and cost of TBI-related disabilities there is a paucity of literature reviewing modern approaches to pharmacotherapy. There is, however, growing evidence that medications may speed recovery by enhancing some neurological functions without impact­ing others.

Pharmacotherapy is in­creasingly being used in both the subacute (less than 1 month post-TBI) and chronic (more than 1 month post-TBI) phases.

Disabilities arising from TBI that have a direct impact on functioning and rehabilitative potential can be broadly classified into four main categories: decreased level of consciousness (LOC), and neuropsychiatric, neurocognitive, and neurobehavioral sequelae.5-8 Decreased level of consciousness refers to a diverse range of clinical states including coma, vegetative states, akinetic mutism, and locked-in states.

Neuropsychiatric symp­toms may present as mood disorders, posttraumatic stress disorder, and personality changes characterized by disinhibition and egocentricity. Neurocognitive injuries vary, but most frequently involve impaired attention, memory, and executive functioning.

Neurobehavioral deficits distinct from neuropsychiatric sequelae may take the form of irritability, hyperexcitability, nervousness, disinhibition, poor impulse control, restlessness, and aggression, with aggression and agitation seen in as many as 30% of brain-injured patients.[5-8]

Depending on the location of in­jury, damage can occur to a variety of neurotransmitter networks critical to cognitive processes. Investigation has focused on the loss of dopaminergic neurons that regulate executive functioning, as well as deficits in norepinephrine and acetylcholine, which limit attention—a critical function for effective rehabilitation.[9]

Fortunately, a number of pharmacological interventions show promise in helping patients cope with these losses and deficits.

Although insufficient evidence exists to establish guidelines for optimal pharmocotherapy, medications may be used to support recovery. Examples are shown in the accompanying Table, which summarizes the pharmacological approaches discussed in more detail below.

When problematic TBI symptoms are identified, clinicians can use this information to determine pharmacological options and integrate them with nonpharmacological options such as physical therapy, occupational therapy, physiatry, and the patient’s support network.

Planning a pharmacological intervention strategy
The decision to use pharmacological intervention should be the result of multidisciplinary collaboration and made with the patient or his or her substitute decision maker. Goals of therapy should be clarified, and outcomes and adverse events should be reliably tracked, particularly so medications that are ineffective or cause adverse events can be discontinued and unnecessary polypharmacy can be avoided.

Selecting the most appropriate agent requires careful analysis of the neurological disabilities present, the nature of the underlying lesion, and the time elapsed since the injury.

Psychostimulants
Psychostimulants such as methylpheni­date are most commonly used to treat attention deficit hyperactivity disorder (ADHD), a condition that involves problems with executive functioning and can be characterized as similar to brain injury both in terms of symptoms and neurotransmitter aberrations.[10]

Although the complete mechanism of action of methylphenidate remains unknown, this agent is thought to bind dopamine transporters, thereby blocking reuptake and increasing extracellular dopamine levels, particularly in the frontal cortex.[11] It is also thought to increase norepinephrine and serotonin levels.

In the majority of studies, methylphenidate has been administered  twice daily, either at a fixed dose of 10 to 15 mg or at a dose of 0.3 mg/kg.[12-15]

In the acute phase after a TBI, methylphenidate-treated patients dem­onstrated better attention, concentration, and performance on motor memory tasks at 1 month, but these benefits did not persist at 3 months. Thus, it has been suggested that while methyl­phenidate may shorten recovery time, it does not change morbidity.[12]

In the chronic phase after a TBI, patients have reported improvements in mood, work performance, and alertness, with more limited evidence suggesting an improvement of fluency and selective attention.

The impact of methylphenidate on chronic attention is more ambiguous: one study suggests improvement in long-term processing speed and attention to tasks but not increased sustained attention or decreased susceptibility to distraction.[12]

Two separate studies have suggested methylphenidate is effective in the treatment of agitation and sei­zures,[16,17] while another demonstrated no neurobehavioral benefit.[18]

Despite the accumulation of controlled clinical trials, there is no consensus on the use of stimulants in treating TBI-induced impairments in arousal and motor activity.

It should be noted that one recent review concluded “at present there is insufficient evidence to support routine use of methylphenidate or other amphetamines to promote recovery from TBI,”[19] while another review noted that at least 10 clinical trials have demonstrated a role for methylpheni­date in both adult and pediatric brain injury patients suffering from neurocognitive deficits, particularly in attention, memory, cognitive processing, and speech.[20]

Methylphenidate has a quick onset of action and relatively benign side effect profile, and we believe it to be useful in both the acute and chronic phase of TBI.

Antidepressants
Despite potentially severe consequenc­es, post-TBI psychiatric sequelae are underdiagnosed and undertreated. Fortunately, current evidence suggests that antidepressants can be used to manage both neuropsychiatric and additional neurological deficits persisting from brain injury.

Selective serotonin reuptake inhi­bitors (SSRIs) have been found useful in treating behavioral syndromes in TBI patients, particularly in the subacute stages of recovery[21] but also in chronic settings.

The majority of studies suggest that SSRIs improve neurobehavioral, neurocognitive, and neuropsychiatric deficits, specifically agitation, depression, psychomotor retardation, and recent memory loss; however, most data originates from nonrandomized trials.

Sertraline administered at an average dose of 100 mg daily for 8 weeks has been found to be beneficial for agitation, depressed mood, and deficits in psychomotor speed and recent memory; shorter treatment durations have demonstrated no benefit.[21]

Similarly, 60 mg daily of fluoxetine for 3 months was shown to be effective in the treatment of obsessive-compulsive disorder caused by brain injury.[22] Finally, paroxetine or citalopram, at a dose of 10 to 40 mg daily, was shown by another study to be equally effective in the treatment of pathological crying.[23] None of the re­viewed studies addressed neurocognitive deficits.

The highest concentration of serotonergic and adrenergic fibres is located near the frontal lobes, the most common site of traumatic contusion.[24]

Consequently, these fibres are commonly injured in TBI, suggesting that newer antidepressants with effects on both norepinephrine and serotonin, such as mirtazapine and venlafaxine, may also be effective in the treatment of TBI sequelae; however, clinical data with these agents in TBI is lacking.

Similarly, bupropion increases both dopamine and norepinephrine levels and is a weak inhibitor of serotonin reuptake. At 150 mg daily, this agent has been useful in treating restlessness.[25]

Antiparkinsonian drugs
The antiparkinsonian drugs amantadine, bromocriptine, and levodopa combined with carbidopa (e.g., Sine­met) have varied mechanisms of action, but all ultimately serve to increase dopamine levels in the brain.

Amantadine acts presynaptically to enhance dopamine release or inhibit its reuptake, and can act postsynaptically to increase the number, or alter the configuration of, dopamine re­ceptors.[26] It is also a noncompetitive NMDA receptor antagonist and may provide protection against possible glutamate-mediated excitotoxicity in the context of TBI.[27]

Bromocriptine is a dopamine receptor agonist affecting primarily D2 receptors and to a lesser extent D1 receptors.[28] The use of levodopa and carbidopa in combination directly increases dopamine levels: levodopa becomes dopamine once de­carboxylated, while carbidopa inhibits L-amino decarboxylase, allowing levodopa to reach the central nervous system.[28]

Multiple studies of amantadine at a dose of 100 to 300 mg daily have suggested its effectiveness in both the acute and chronic care phases after TBI, particularly in diffuse, frontal, or right-sided brain injury.

Currently, the evidence suggests neurocognitive or neurobehavioral deficits, particularly cognition difficulties and agitation, are primary indications for amantadine use.[26,29,30]

Amantadine-treated patients demonstrated improvements in motivation; decreased level of apathy; increased attention, concentration, and alertness; improved executive functioning; decreased processing time; reduced agitation, distractibility, fatigue, aggression, and anxiety.

In addition, patients treated with amantadine demonstrated changes in outcome LOC, specifically improved arousal and LOC as measured by the Glasgow Coma Scale. Interestingly, one study also suggested decreased mortality.[31] To date, no study has shown an improvement in memory.

Three case reports using 5 to 45 mg of bromocriptine daily,[32] and one study using a combination of 100 mg of bromocriptine with 100 mg of ephedrine,[33] showed improvement in akinetic mutism, while another study using 5 mg of bromocriptine combined with sensory stimulation led to improvements in patients with vegetative or minimal consciousness.[34]

The evidence is similarly limited for levidopa and carbidopa medications where nonrandomized studies suggest that they might be useful in the chronic phase of TBI with diffuse injury and persistent vegetative state.[35]

Combining agents has also been tried in one study that found improvements in neuropsychiatric deficits with the daily administration of 25 mg/200 mg of levodopa/carbidopa three times daily, 250 mg of amantadine, and 5 mg of bromocriptine twice daily.[36]

Anticonvulsants
Anticonvulsants have been used with varying results for treating symptoms of TBI. Valproic acid, for example, enhances inhibitory control mediated by the neurotransmitter GABA, thereby promoting general central nervous system stabilization, but findings thus far have been mixed.

Investigations utilizing 600 to 2250 mg of valproic acid daily (resulting in serum levels of 40 to 100 µg/mL), have demonstrated positive neurocognitive effects, in­cluding improved recent memory and problem-solving, as well as ameliorating neuropsychiatric and neuro­behavioral symptoms such as depression, mania, destructive and aggressive behavior, restlessness, disinhibition, impulsivity, lability, and alertness.[37-41]

Conversely, one control­led trial found valproic acid negatively impacted decision-making speed, and another suggested an increased mortality rate with valproic acid use.[37-41]

Other agents
Modafinil is a vigilance-promoting drug commonly used to treat narcolepsy and idiopathic hypersomnia, illnesses that can present with symptoms similar to those seen in TBI: excessive daytime sleepiness, inattention, and decreased ability to perform social activities.

The precise mechanism of action remains unknown, although it is believed that modafinil can inhibit GABA or increase glutamate levels in the nondopaminergic anterior hypothalamus, hippocampus, and amygdale.[42,43]

Two studies that investigated the role of modafinil in chronic TBI showed an improvement in neurocognitive deficits, specifically memory and attention, as well as improving daytime somnolence at doses between 100 and 400 mg.[44,45]

Four randomized control trials examining the use of beta-blockers, specifically propranolol and pindolol, have demonstrated beneficial effects on neurobehavioral symptoms of ag­gression and agitation in both the chronic and subacute phase. This class of drugs deserves further attention for the management of both neuropsychiatric and neurobehavioral sequelae of TBI.[46]

Neuroleptics are being used in­creasingly in the setting of delirium, and one might consider using them in an attempt to allow the brain to recalibrate neurotransmitter levels. However, it should be noted that there is some evidence that dopamine blockade may negatively affect recovery.[47,48]

There are also a number of animal studies examining drugs that have the potential to adversely affect brain recovery following TBI. These studies typically use a stroke model, so generalizing to TBI may not be possible.

Nevertheless, the evidence currently does not support the use of neuro­leptics, benzodiazepines, phen­y­toin, prazosin, trazodone, and similar agents because of their potential adverse effect on recovery, presumably through the impacts they have on neurotransmitters such as dopamine, norepinephrine, or GABA.[49-51]

Preliminary evidence suggests cho­linesterase inhibitors such as don­epezil may improve long-term cognitive outcomes, particularly in domains such as memory and attention when administered early, and further in­vestigation with these agents is also warranted.[52,53]

Finally, antiandrogenic medications, such as estrogen and medroxyprogesterone, may have a role to play in reducing inappropriate sexual be­havior in patients with TBI. In a case study and one small trial, these drugs demonstrated effectiveness.[54]

Summary
The nature of TBI sequelae, whether psychiatric, cognitive, or behavioral, is poorly understood. Likewise, the use of pharmacological interventions to improve symptoms, function, and outcome is still under development.

There are, however, a number of agents that inspire optimism. When treating neurological deficits medically, there is evidence to support the tailored use of these agents for particular TBI clinical scenarios. The timing and nature of symptoms, along with wheth­er agents are administered in the acute or chronic phase after TBI, are all relevant factors for determining proper use.

With insufficient evidence to establish guidelines for optimal treatment, care must be taken when choosing pharmacological interventions for TBI.

If the decision is made to use medications to promote TBI recovery or treat its attendant disabilities, clinicians should thoroughly document the goals of pharmacotherapy and closely monitor for side effects. Future studies will undoubtedly add to the clinician’s armamentarium for the care of TBI patients.

Competing interests
None declared.


ReferencesTop

1. Bruns J Jr, Hauser WA. The epidemiology of traumatic brain injury: A review. Epilepsia 2003;44:2-10.
2. Okie S. Traumatic brain injury in the war zone. N Engl J Med 2005;352:2043-2047.
3. Thurman DJ, Alverson C, Dunn KA, et al. Traumatic brain injury in the United States: A public health perspective. J Head Trauma Rehabil 14 1999;14:602-615.
4. Woo BH, Nesathurai S (eds). The rehabilitation of patients with traumatic brain injury. Malden, MA: Blackwell Science; 2000:5-12.
5. Bricolo A. Prolonged posttraumatic coma, In: Vinken PJ, Bruyn GW (eds). Handbook of clinical neurology Amsterdam: Elsevier; 1976:699-755.
6. O’Dell MW, Riggs RV. Management of the minimally responsive patient. In: Horn LJ (ed). Medical rehabilitation of traumatic brain injury. Philadelphia: Hanley and Belfus; 1996:103-131.
7. Salmond CH, Sahakian BJ. Cognitive outcome in traumatic brain injury survivors. Curr Opin Crit Care 2005;11:111-116.
8. Hellawell DJ, Taylor RT, Pentland B. Cognitive and psychosocial outcome following moderate or severe traumatic brain injury. Brain Inj 1999;13:489-504.
9. Arciniegas DB, The cholinergic hypothesis of cognitive impairment caused by traumatic brain injury. Curr Psychiatry Rep 2003;5:391-399.
10. Evans RW, Gualtieri CT. Psychostimulant pharmacology in traumatic brain injury. J Head Trauma Rehabil 1987;2:29-33.
11. Challman T, Lipsky J. Methylphenidate: Its pharmacology and uses. Mayo Clin Proc 2000;75:711-721.
12. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. Am J Phys Med Rehabil 1997;76:440-450.
13. Kaelin C, Cifu D, Matthies B. Methyl­phenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil 1996;77:6-10.
14. Speech T, Rao S, Osmon D, et al. A double blind controlled study of methylphen­idate treatment in closed head injury. Brain Inj 1993;7:333-338.
15. Plenger P, Dixon E, Castillo R, et al. Subacute methylphenidate treatment for moderate to moderately severe traumatic brain injury: A preliminary double-blind placebo-controlled study. Arch Phys Med Rehabil 1996;77:536-540.
16. Mooney G, Haas L. Effect of methyl­phen­i­date on brain injury-related anger. Arch Phys Med Rehabil 1993;74:153-160.
17. Wroblewski B, Leary J, Phelan A, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry 1992;53:86-89.
18. Evans R, Gualtieri T, Patterson D. Treatment of chronic closed head injury with psychostimulant drugs: A controlled case study and an appropriate evaluation procedure. J Nerv Ment Dis 1987;175:110.
19. Forsyth R, Jayamoni B. Noradrenergic agonists for acute traumatic brain injury. Cochrane Database Syst Rev 2003;(1):CD003984.
20. Siddall OM, Use of methylphedinate in traumatic brain injury. Ann Pharmacother 2005;39:1309-1313.
21. Meythaler J, Lawrence D, Devivo M, et al. Sertraline to improve arousal and alertness in severe traumatic brain injury secondary to motor vehicle crashes. Brain Inj 2000;15:321-331.
22. Stengler-Wenzke K, Muller U. Fluoxetine for OCD after brain injury. Am J Psychiatry 2002;159:872.
23. Muller U, Mural T, Bauer-Wittmund T, et al. Paroxetine versus citalopram treatment of pathological crying after brain injury. Brain Inj 1999;13:808-811.
24. De Marchi R, Bansal V, Hung A, et al. Review of awakening agents. Can J Neurol Sci 2005;32:4-17.
25. Teng C, Bhalerao S, Lee A, et al. The use of buproprion in the treatment of restlessness after a traumatic brain injury. Brain Inj 2001;15:463-467.
26. Schneider W, Drew-Cates J, Wong T, et al. Cognitive and behavioural efficacy of amantadine in acute traumatic brain injury: An initial double-blind placebo-controlled study. Brain Injury 1999;13:863-872.
27. Kraus M, Maki P. The combined use of amantadine and l-dopa/carbidopa in the treatment of chronic brain injury. Brain Inj 1997;11:455-460.
28. Zafonte R, Lexell J, Cullen N. Possible applications for dopaminergic agents following traumatic brain injury: Part 1. J Head Trauma Rehabil 2000;15:1179-1182.
29. Meythaler J, Brunner R, Johnson A, et al. Amantadine to improve neurorecovery in traumatic brain injury-associated diffuse axonal injury: A pilot double-blind randomized trial. J Head Trauma Rehabil 2002;31:300-313.
30. Zafonte R, Watanabe T, Mann N. Amantadine: A potential treatment for the minimally conscious state. Brain Inj 1998;12:617-621.
31. Saniova B, Drobny M, Kneslova L, et al. The outcome of patients with severe head injuries treated with amantadine sulphate. J Neur Transm 2004;111:511-514.
32. Crismon M, Childs A, Wilcox R, et al. The effect of bromocriptine on speech dysfunction in patients with diffuse brain injury (akinetic mutism). Clin Neuropharmacol 1988;11:462-466.
33. Anderson B. Relief of akinetic mutism from obstructive hydrocephalus using bromocriptine and ephedrine. J Neurosurg 1992;76:152-155.
34. Passler M, Riggs R. Positive outcomes in traumatic brain injury-vegetative state: Patients treated with bromocriptine. Arch Phys Med Rehabil 2001;82:311-315.
35. Haig A, Ruess J. Recovery from vegetative state of six months’ duration associated with Sinemet (levodopa/carbidopa). Arch Phys Med Rehabil 1990;71:1081-1082.
36. Karli D, Burke D, Kim H, et al. Effects of dopaminergic combination therapy for frontal lobe dysfunction in traumatic brain injury rehabilitation. Brain Inj 1999;13:63-68.
37. Wroblewski B, Joseph A, Kupfer J, et al. Effectiveness of valproic acid on destructive and aggressive behaviours in pa­tients with acquired brain injury. Brain Inj 1997;11:37-47.
38. Massagli T. Neurobehavioral effects of phenytoin, carbamazepine, and valproic acid: Implications for use in traumatic brain injury. Arch Phys Med and Rehabil 1991;72:219-225.
39. Dikmen S, Machamer J, Winn H, et al. Neuropsychological effects of valproate in traumatic brain injury. Neurology 2000;54:895-902.
40. Chatham-Showalter P, Kimmel DN. Agitated symptom response to divalproex following acute brain injury. J Neuropsychiatry Clin Neurosci 2000;12:395-397.
41. Kim E, Humaran T. Divalproex in the management of neuropsychiatric complications of remote acquired brain injury. J Neuropsychiatry Clin Neurosci 2002;14:202-205.
42. Lin J, Hou Y, Jouvet M. Potential brain neuronal targets for amphetamine-, methylphenidate-, and modafinil-induced wakefulness, evidenced by c-fos im­muno­cytochemistry in the cat. Proc Natl Acad Sci U S A 1996;93:14128-14133.
43. Ferraro L, Antonelli T, Tanganelli S. The vigilance promoting drug modafinil in­creases extracellular glutamate levels in the medial preoptic area and the posterior hypothalamus of the conscious rat: Prevention by local GABAA receptor blockade. Neuropsychopharmacology 1999;20:346-356.
44. Saletu B, Saletu M, Grunberger J, et al. Treatment of the alcoholic organic brain syndrome: Double-blind, placebo-controlled clinical, psychometric and electroencephalographic mapping studies with modafinil. Neuropsychobiology 1993;27:26-39.
45. Teitelman E. Off-label uses of modafinil. Am J Psychiatry 2001;158:1341.
46. Fleminger S, Greenwood RJ, Oliver DL. Pharmacological management for agitation and aggression in people with acquired brain injury. Cochrane Database Syst Rev 2003;(1):CD003299.
47. Feeney DM, Gonzalez A, Law WA. Amphetamine, haloperidol and experience interact to affect the rate of recovery after motor cortex injury. Science 1982;217:855-857.
48. Goldstein LB. Common drugs may influence motor recovery after stroke. Neurology 1995;45:865-872.
49. Schallert T, Hernandez T, Barth T. Recovery of function after brain damage: Severe and chronic disruption by diaze­pam. Brain Res 1986;379:104-111.
50. Brailowsky S, Knight RT, Efron R. Phenytoin increases the severity of cortical hemiplegia in rats. Brain Res 1986;376:71-77.
51. Goldstein LB. Influence of common drugs and related factors on stroke outcome. Curr Opin Neurol 1997;10:52-57.
52. Zhang L, Plotkin RC, Wang G, et al. Cholinergic augmentation with donepezil enhances recovery in short-term memory and sustained attention after traumatic brain injury. Arch Phys Med Rehabil 2004;85:1050-1055.
53. Walker W, Seel R, Gibellato M, et al. The effects of donepezil on traumatic brain injury acute rehabilitation outcomes. Brain Inj 2004;18:739-750.
54. Levy M, Berson A, Cook T, et al. Treatment of agitation following traumatic brain injury: A review of the literature. NeuroRehabilitation 2005;20:279-306.

Source: Pharmacological interventions for traumatic brain injury | BC Medical Journal

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[WEB SITE]  – Neurobehavioral Rehabilitation – CNS

Changes in personality and behavior are familiar consequences of traumatic brain injury (TBI) and often represent a significant barrier to effective rehabilitation and a successful outcome. In the acute stages of recovery from TBI, it is common for a person to exhibit a variety of behavioral complications which are considered by many to be a normal phase of recovery. When these behaviors continue beyond the acute recovery phase, however, and form on-going negative patterns of interaction with others, very specialized treatment is required. These behaviors can be disturbing to families and staff, disruptive to therapy, jeopardize patient safety and negatively impact a patient’s community re-entry and future quality of life.

 

Applied Behavior Analysis

Applied behavior analysis can be a powerful methodology for teaching people more positive ways of interacting with their environment and those around them. Centre for Neuro Skills provides a staff of Board Certified Behavior Analysts and over thirty-five years of experience in successfully treating patients with the most severe behavioral complications following their brain injury. Our behavior analysts complete in-depth assessments and detailed treatment plans to reduce challenging behaviors and increase positive behaviors. Staff members at both our clinic and residential locations are trained in behavior skills, crisis prevention, implementation of behavioral programming and regularly meet with behavior analysts to discuss the effectiveness of treatment plans.

 

Neurobehavioral Rehabilitation Program

Centre for Neuro Skills treats a variety of challenging and severe behaviors including:

  • Physical Aggression
  • Verbal Aggression
  • Self-Injurious Behavior
  • Lack of Initiation
  • Inappropriate Social Behavior
  • Noncompliance
  • Sexual Disinhibition
  • Property Destruction
  • Escape and Elopement

 

Our Neurobehavioral Rehabilitation Program is based on fundamentals of behavior analysis, such as precisely identifying a patient’s challenging behaviors, any environmental and internal factors that might be contributing to the occurrence of the behaviors and responses to the behaviors that make it more likely to continue. Neurobehavioral treatment is most effective when it is integrated with a comprehensive brain injury rehabilitation program. Centre for Neuro Skills provides coordinated medical and behavioral programming so as to maximize learning and reduce reliance upon medication, however, some patients are optimized by a combination of the two. Neurobehavioral treatment provides a “meta-structure” within which the various therapeutic disciplines of brain injury rehabilitation are carried out. The goal is to reduce those behaviors that limit independence and increase positive behaviors that empower a person and enhance opportunities for community, social, and family interaction.

 

Neuro Behavior Program Emphasizes Community Re-Integration: Read more

Case Study: Overcoming Behavioral Struggles, a Woman Embraces Life Again: Read more

TBI and Behavior Articles: Read abstracts

 

CNS Behavior Publications

The use of noncontingent reinforcement and contingent restraint to reduce physical aggression and self-injurious behaviour in a traumatically brain injured adult, Persel, C.S. and Persel, C.H. (1997), Brain Injury, 11(10), 751-60. Read abstract

Persel, C.S., & Persel, C.H. (2010). The Use of Applied Behavior Analysis in Traumatic Brain Injury Rehabilitation. In M.J. Ashley (Editor), Traumatic Brain Injury: Rehabilitation, Treatment and Case Management. Third Edition. Boca-Raton, FL: CRC Press Inc. Read more

 

Neurobehavioral Treatment of Severe Behavior After Traumatic Brain Injury

Source: Traumatic Brain Injury Resource Guide – Neurobehavioral Rehabilitation

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[WEB SITE] Traumatic Brain Injury Resource Guide – Neurobehavioral Rehabilitation

Neurobehavioral Rehabilitation

Changes in personality and behavior are familiar consequences of traumatic brain injury (TBI) and often represent a significant barrier to effective rehabilitation and a successful outcome. In the acute stages of recovery from TBI, it is common for a person to exhibit a variety of behavioral complications which are considered by many to be a normal phase of recovery. When these behaviors continue beyond the acute recovery phase, however, and form on-going negative patterns of interaction with others, very specialized treatment is required. These behaviors can be disturbing to families and staff, disruptive to therapy, jeopardize patient safety and negatively impact a patient’s community re-entry and future quality of life.

 

Applied Behavior Analysis

Applied behavior analysis can be a powerful methodology for teaching people more positive ways of interacting with their environment and those around them. Centre for Neuro Skills provides a staff of Board Certified Behavior Analysts and over thirty-five years of experience in successfully treating patients with the most severe behavioral complications following their brain injury. Our behavior analysts complete in-depth assessments and detailed treatment plans to reduce challenging behaviors and increase positive behaviors. Staff members at both our clinic and residential locations are trained in behavior skills, crisis prevention, implementation of behavioral programming and regularly meet with behavior analysts to discuss the effectiveness of treatment plans.

 

Neurobehavioral Rehabilitation Program

Centre for Neuro Skills treats a variety of challenging and severe behaviors including:

  • Physical Aggression
  • Verbal Aggression
  • Self-Injurious Behavior
  • Lack of Initiation
  • Inappropriate Social Behavior
  • Noncompliance
  • Sexual Disinhibition
  • Property Destruction
  • Escape and Elopement

 

Our Neurobehavioral Rehabilitation Program is based on fundamentals of behavior analysis, such as precisely identifying a patient’s challenging behaviors, any environmental and internal factors that might be contributing to the occurrence of the behaviors and responses to the behaviors that make it more likely to continue. Neurobehavioral treatment is most effective when it is integrated with a comprehensive brain injury rehabilitation program. Centre for Neuro Skills provides coordinated medical and behavioral programming so as to maximize learning and reduce reliance upon medication, however, some patients are optimized by a combination of the two. Neurobehavioral treatment provides a “meta-structure” within which the various therapeutic disciplines of brain injury rehabilitation are carried out. The goal is to reduce those behaviors that limit independence and increase positive behaviors that empower a person and enhance opportunities for community, social, and family interaction.

 

Neuro Behavior Program Emphasizes Community Re-Integration: Read more

Case Study: Overcoming Behavioral Struggles, a Woman Embraces Life Again: Read more

TBI and Behavior Articles: Read abstracts

 

CNS Behavior Publications

The use of noncontingent reinforcement and contingent restraint to reduce physical aggression and self-injurious behaviour in a traumatically brain injured adult, Persel, C.S. and Persel, C.H. (1997), Brain Injury, 11(10), 751-60. Read abstract

Persel, C.S., & Persel, C.H. (2010). The Use of Applied Behavior Analysis in Traumatic Brain Injury Rehabilitation. In M.J. Ashley (Editor), Traumatic Brain Injury: Rehabilitation, Treatment and Case Management. Third Edition. Boca-Raton, FL: CRC Press Inc. Read more

 

Neurobehavioral Treatment of Severe Behavior After Traumatic Brain Injury

Source: Traumatic Brain Injury Resource Guide – Neurobehavioral Rehabilitation

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[ARTICLE] Post-Hospital Brain Injury Rehabilitation: Comparison of Neurobehavioral Intensity and Neurorehabilitation Outcomes

…Participation in the comprehensive post-hospital rehabilitation programs lead to significant reduction in disability for both groups.Significant disability reduction was demonstrated within the NB group which is remarkable since this group is chronically impaired, averaging 8.3 years post injury at the time of study inclusion, with behavioral dyscontrol…

via Post-Hospital Brain Injury Rehabilitation: Comparison of Neurobehavioral Intensity and Neurorehabilitation Outcomes – Archives of Physical Medicine and Rehabilitation.

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