The Agitated Client and More: Managing Neurobehavioral Issues in Clients with Brain Injury
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The Agitated Client and More: Managing Neurobehavioral Issues in Clients with Brain Injury
- 1. The Agitated Client and More: Managing Neurobehavioral Issues in Clients with Brain Injury NRH / ReMed / BIA of DC Joint Conference 10/27/11 Scott Peters, MS, OTR/L
- 17. Neurobehavioral Programming Elements Stable Activity Pattern Establish Medical Stability Behavioral Stability
- 20. Comparing Terminology (Trepacz and Kennedy, 2005) Coma Stupor Delirium Amnestic Disorder Recovery Post Traumatic Amnesia Post Traumatic Agitation Time Post Injury
- 52. Brief Review and Concluding Thoughts Stable Activity Pattern Establish Medical Stability Behavioral Stability PTA Aggression Mood Disorders Diminished Motivation Post Traumatic Psychosis Sexually Aberrant Behavior
- 53. Any Questions?
Notas do Editor
- Neurobehavioral Changes among brain injury survivors remains significantly problemmatic for families, caregivers and rehabilitation professionals. Studies have shown that increased irritability and aggressive behaviors are frequent and persistant sequelae of aquired brain injury. Approached this topic from a perspective of the types of clients that ReMed has worked with over the past 25 years that fall into the category of behavioral clients. Issues of aggression, depression, anxiety, mood instability, sexual disinhibition, amotivation, PTA with resultant confusion are generally evident in the individuals that are referred to us. Usually these issues have been treated in a hospital setting or an outpatient setting yet they continue to persist leading to concerns about safety, family capacity to handle their loved ones, etc. The mission of providing services to this very challenging populations has been a consistent component of ReMed’s mission for the past 25 years. I am the clinical director of ReMed’s Short Term and Intensive Residential Services. I have been involved in programming for TBI survivors with Neurobehavioral issues for the 19 years that I have been with ReMed. I am an OT by training so I had to rely on really smart clinicians that ReMed has always been committed to hire and retain to help me understand effective approaches to address the challenging sequelae of our clients. In preparation fo the this presentation I attempted to review literature summarized from the past quarter of a century since ReMed has been around. I will be presenting you, an experienced group of professionals, with information related to Neurobehavioral changes following TBI.
- Pos Rf candy for answering, paycheck, etc… Neg Rf bringing umbrella, headphones at library, etc… Pos Punish aversive stimuli, circling no on schedule Neg Punish Time-Out, loss of privileges, etc...
- These terms are loosely used and have often been used interchangeably. Delirium can be caused by a wide variety of medical, pharmacological and postoperative conditions. From 10% to 30% in general hospital patients (Fann 2000). Some surgical populations even greater (as much as 50% in elderly hip patients) (Williams et al. 1985). Post Traumatic Amnesia also defined as a “period of clouded consciousness which precedes the attainment of full orientation and continuous awareness in persons recovering from head injury. Also “characterized primarily by a failure of amnestic processes (Mandelberg 1975). Katz (1992) recognized the confusional state embedded in PTA. Stuss et al.1999 called it postraumatic confusional state. PTA is generally considered during the time of recovery continuum after coma, emerging from stupor, including delirium and amnestic disorder
- Patients may progress without going through the stages in a regimented manner. Delirium may have a hypoactive, hyperactive or mixed motoric presentation. These presentations may include behavioral symptoms including yelling, punching and mood lability. Post traumatic agitation overlaps with the hyperactive type of delirium. In a study conducted by Tate et al. 2000 of severly brain injured patient, it was found that disorientation subsided before amnesia in 94% of the cases. Therefore, as delirium resolves, orientation improves and some form of memory impairment could persist. In a study of behavioral disturbances after TBI showed that restlessness and agitation resolved in all patients before the resolution of PTA (indicating that there is a restlessness phase to delirium.
- These symptoms can have an abrupt onset, fluctuating course and it is usually reversible.
- Drug Intoxication: Anticholinergics, histamine antagonists, opiods, barbituates, etc. Drug Withdrawal: alchohol, benzodiazipines, barbiturates Metabolic: dehydration, hepatic or renal insufficiency, hyper – hypoglycemia Infection: abcess, encephalitis, etc. Endocrine: hypothyroidism, Seizures: ictal and postictal states Cancer: metastases, brain tumor Vascular: stroke, TIA, shock, MI, etc, Environmental: heat stroke, toxins, carbon monoxide
- Environmental Structuring: Safety Management : one to one’s, items in room, falls risk, wander risk Sensory Stimulation Level: low stim as possible, structure number of visitors, amount of information given, etc. Environment: orienting materials posted, review of orienting materials, clock, calendar, pictures, video from family, logbook, calming / soothing activities (music, TV, games) Staff Approach: critical (reassuring, soothing, redirecting, reorienting); consistent information delivered in a consistent manner, specific approaches trialed for care needs; pick your battles (shower, toilet, medications) Neuroleptics: Haldol, side effect of sedation, TD Dopamine blocking effects of Haldol may negatively impact cognitive rehab efforts (Feeney et al. 1982; Gualtieri 1991) because dopaminergic medications enhance memory (Gualtieri 1991). Atypicals: side effect profiles more tolerable. Clozapine (Ratey et al. 1993), olanzapine (Edell and Tunis 2001; Kinon et al. 2001; Meehan et al. 2001, 2002; Wright et al. 2001) and risperidone (Czobor et al. 1995) have been effective in reducing aggression related to their effects on seratonin receptors. Benzodiazepines can worsen delirium and further impair cognition so are usually avoided.
- Norepinephrine: Major NE tracts in the brain are vulnerable to TBI. Studies have shown that elevations of plasma Norepinephrine are evident (Clifton et al. 1981;Hamill et al. 1987). Animal studies suggest that NE enhances aggressive behavior. Humans who have exhibit aggressive or impulsive behaviors have been shown to have increased NE metabolite (G.L. Brown et al. 1979). Serotonergic neurons originate in the pons and upper brainstem and project to the frontal cortex. Changes in serotonin activity have been found in patients with TBI. Animal studies suggest lowered levels of serotonin have been associated with increased aggression including studies of predatory aggression. Studies have confirmed the role in decreased serotonin in the expression of aggression and impulsivity in humans (Kruesi et al.1992; Lonnoila and Virkkunen 1992) particularly as it applies to self destructive acts. Dopamine systems are prominent in mesolimbic systems and mesocortical regions. Elevated serum dopamine levels have been correlated with severity of injury and poorer outcomes (Hamill et al. 1987). Increases in dopamine may lead to aggression in several animal models (Eichelman 1987). Cholinergic complex is found in the basal forebrain area. Elevated acetylcholine has been found in fluid obtained from intraventricular catheters or lumbar punctures in patients after TBI (Grossman et al. 1975). Acetylcholine has been found to increase aggressive behaviors. GABA is an inhibitory neurotransmitter found throughout he brain. Currently no studies have examined GABA levels after brain injury but it is expected that injured neurons would produce less GABA. Increasing GABA via benzodiezapines results in reduced aggressive behavior in animals (Eichelman 1987).
- Neuropsychiatric Problems: Learning Disabilities Attentional Deficits] Behavioral Problems Personality Disorders Preinjury History of Substance Abuse: associated with aggressive behavior 6 months after TBI (Tateno et al. 2003) Coexisting anxiety and depression: associated with increased aggression and irritability (Hibbard et al. 1998; Tateno et al. 2003) 56% of TBI with Depression demonstrated verbal and physical aggression compared with 22% of TBI clients who did not have a mood disorder
- Alcohol: most commonly associated with aggression (intoxication and withdrawal). Positive BAL when injured – longer periods of agitation as compared to those with no BAL (Sparadeo and Gill 1989) Intoxication following ABI results in dysregulation of behaviors Stimulating Drugs (Cocaine and Amphetamines): may produce severe anxiety and aggression, may lead to manic state and paranoid ideation in latter stages Steriods: prednisone, cortisone and anabolic steriods Antidepressants: may contribute to agitation in early stages of treatment (our experience with long term behavioral clients) Antipsychotics: may induce agitation through anticholinergic side effects, agitation accompany akathesia Analgesics: opiates and other narcotics, contribute to intoxication and withdrawal states Anticholinergic Drugs: including over the counter sedatives associated with delirium and central anticholinergic syndrome
- Studies have shown an increase in hostility, irritability and aggression interictally (Mendez et al. 1987; Robertson et al . 1987)
- No medication has been approved by FDA for treatment of aggression… must use medications approved for other uses. Antipsychotics: in acute phase employed for the sedative effects, neuroleptics risk of side effects (tardive dyskinesia or akathisia). Studies in acute phase suggest that decreasing dopamine may prolong periods of PTA. Consider atypicals. For chronic aggression consider if also treating psychotic symptoms Sedatives and Hypnotics: use of benzodiazapines in management of acute aggression (amplify’s inhibitory neurotransmitter GABA. Negative impact on memory function, coordination and balance. Antianxiety: seratonin is a key neurotransmitter in the modulation of aggressive behavior (Gaultieri 1991a, 1991b; Levine 1988). Some instances more aggressive with antianxiety meds (buspar, Klonopin) Anticonvulsants: studies indicate carbamazepine effective (Yudofsky et al. 1998); valproic acid (Geracioti 1994; Giakas et al. 1990; Mattes 1992); Gabapentin has also been found to be beneficial (Hermann et al. 2000; Roane et al. 2000) Antimanic: lithium has been widely used and has been found to be effective. Our experience with long term lithium use (kidney failure), replace with other agents (atypicals) Antidepressants: studies have shown antidepressants that act preferentially (Elavil) or specifically (Prozac) on seratonin have been found to be effective. Trazadone found to be effective in treatment of aggression (Yudofsky et al.1998). Our experience is that use of antidepressants can be tricky. Put in place a mood stabilizer first to buffer against manic side effects. Stimulants: some studies about the use of dopaminergic medications on treatment of agitation and aggression. Amantadine and Methylphenidate. We are very wary. Antihypertensives: several studies about the use of beta blockers (Propranolol, Nadolol and Pinolol) (Yudofsky et al. 1998).
- Depressive disorders and anxiety are frequent complications among patients with TBI. Variability of frequency in study results due to lack of uniformity in the psychiatric diagnosis and reliance on rating scales or relatives reports rather than structured interviews of the patients and established diagnostic criteria ie DSM – IV - TR (American Psychiatric Association 2000). Hibbard et al. 1998: 61% - used a structured interview and DSM- IV criteria sample size 100 adults with TBI evaluated 8 years (on average) after trauma. Kruetzer et al. 2001: 42% - sample size of 722 outpatients who were on average 2.5 years after brain injury Koponen et al. 2002: 26% - sample size 60 TBI patients who were followed for an average of 30 years Data suggests that there is a significant risk for ongoing depression following TBI
- Suicidal ideation, suicide attempts and completed suicides occur more frequently in patients with TBI compared with non brain injured control subjects (Oquendo et al. 2004; Silver et al.2001; and Engberg 2001)
- Anxiety : studies conducted to determine frequency and types of anxiety disorders following TBI. Likely that a combination of factors including neuroanatomic correlates between TBI and anxiety disorders, psychosocial consequences of disability and a biologic vulnerability for anxiety. In a study by Fann et al. 2000 evaluated 50 consecutive TBI patients (university TBI program, average 3 years post, mostly mild TBI) found 24% had GAD with patients also having major depressive disorder. However it was noted that 34% had a history of GAD (difficult to determine if GAD was because of TBI). Another study by Salazar et al. 2000 evaluated 120 consecutive active duty military members with moderate to severe TBI. 10% had generalized anxiety at baseline and 15% at one year. Therefore study suggests that anxiety is common but link between TBI and anxiety is unclear. Areas implicated in the neurobiology of anxiety include diffuse brain injury, frontal and temporal structures (Levin and Krauss 1994) including the hippocampus and the amygdala (Bigler 2001). These are consistent with TBI. Physiologic response includes increased levels of cortisol and catecholamines to ready for “fight or flight” response and cortisol to negatively impact the hypothalamus and pituitary attempts to shut down the stress response. The amygdala and hippocampus are located close to the temporal lobes. Frontal and temporal lobes are often affected by trauma and due to the close proximity of the amygdala, amygdala and hippocampus is often involved in TBI related anxiety disorders. Injuries to these structures may predispose patients to the development of anxiety symptoms following TBI. PTSD: required for this diagnosis is experience of a traumatic event that later evokes physiological reactivity, emotional distress upon reminders of the event, and reexperiencing phenomena (e.g. flashbacks, nightmares and intrusive thoughts of the traumatic event. Anxiety has been described in the literature for some time, PTSD is more unclear (controversial) with the issue of neurogenic amnesia for the event protecting the patient from developing memories and future symptoms of flashbacks and nightmares. Studies have shown TBI patients who developed PTSD typicially had brief or no LOC. In a study by Sbordone and Liter (1995) compared individuals with PTSD with another group who had PCS. None with PTSD had LOC while 24 of 28 with PCS had LOC and could not give a detailed account of the trauma. No individual had both PTSD and PCS leading the authors to conclude that the two do not occur simultaneoulsy. Summary of the studies suggest that PTSD after TBI does occur but may be modified by the brain injury. Intrusive memories are less common than in non – TBI populations and in less severely injured individuals with TBI. Can develop PTSD related to memories of events following the injury (respond to a story of the event, photograph of the accident, seeing injuries associated with the event. PTSD can also be related to events immediately before the LOC and traumas reactivated from earlier life events. Neuroimaging studies suggest that in non TBI patients, involvement of the limbic structures including amygdala, hippocampus suggest vulnerability to PTSD following TBI (Bigler 2001). Mania and hypomnia: has been reported in a number of organic disorders such as thyroid disorders, uremia, Vitamin B12 deficiency as well as brain tumors, central nervous systems dysfunction, stroke (Cummings and Mendez 1984) and TBI (Bamrah and Johnson 1980). Shukla et al. 1987 reported on 20 patients who developed manic syndromes following TBI. They found a significant association between mania and post traumatic seizures but no association with a family history of bipolar disorder among 85 first degree relatives. Jorge et al. 1993 studied manic syndromes in 66 TBI patients. Six patients (9%) developed secondary mania. Manic episodes lasted approximately 2 months but expansive mood had a mean period of 5.7 months. Secondary mania was not related to severity of brain injury, degree of physical or intellectual impairment, level of social functioning or history (family or personal) of psychiatric history. Did appear to be related to presence of basopolar temporal lesions.
- Literature suggests there is a lack of adequately controlled clinical studies to provide a solid scientific basis for neuropsychiatric treatment. Continue to employ anecdotal cases and clinical experience to guide treatment decisions Tricyclics have important anticholinergic effects that may interfere with cognitive and memory functions and may lower the seizure threshold. However nortryptaline (Pamelor) is a reasonable choice with close monitoring blood levels and toxic effects. SSRI’s: selective seratonin reuptake inhibitor appears to have less adverse side effect profile. This includes citalopram (Celexa), sertraline (Zoloft), paroxetine (Paxil) venlafaxine (Effexor), fluoxetine (Prozac). Commonly used in TBI populations to treat anxiety symptoms. One study showed a 50% improvement in depressive symptoms in the treatment of 15 TBI patients diagnosed with major depression after TBI (Fann et al. 2000). Side effects can include apathy and sexual dysfunction. Psycho – Stimulants: dextroamphetamine (Dexadrine) and methylphenidate (Ritalin) (Zasler 1992). Must monitor closely for side effects (anxiety, dysphoria, irritability, insomnia, mania). Amantadine has been found to have some positive effects for treatment of motivational deficits. Aricept (Donepenzil) empirical evidence of the beneficial effects on cognitive functioning, motivation and general well being. Our experience has also included Provigil to promote wakefulness (sleep disorder such as narcolepsy) Anxiolytics: Buspirone (Buspar) can be considered, a seratonin 1A agonist. Ancedotal reports suggest that Buspar may have positive effects with aggression and agitiation. May be good as an add on med with panic disorders. Avoid the use of Benzodiazipines due to excessive sedation, negative impact on cognition (attention and memory) and the risk for abuse / dependence issues if used for extended periods. Mood Stabilizers / Anticonvulsants: may be helpful in the treatment of anxiety related to manic symptoms or agitation related to TBI. Limited evidence in the literature about the effectiveness of Depakote and Neurontin for anxiety although Lamictal (Lamotrigine) may benefit patients with PTSD. Anticonvulsants may be a reasonable treatment for anxiety associated with aggression. ECT Electroconvulsant therapy: may be considered if intractible depression that does not respond to other efforts. Recent experience with two clients that came to us with having been previously treated with ECT. Both cases did not have great outcomes with us. Issue was long standing history of depression / suicidal ideation, rigid thinking (from TBI) and recent emotional activation. Recent Case Individual came in with preinjury history of depression and sustained TBI secondary to an assault. Symptoms included anxiety, depression, cognitive impairment including attention, concentration and memory. Had been psychiatrically hospitalized for depression. Current medications were Prozac, Klonopin and Seroquel. Suspicion of alcohol abuse. Goal was to return to some form of employment. Plan: Discontinue Klonopin via a gradual schedule. Klonopin considered sedating, addicting and contributing to cognitive suppression. Replace the Seroquel as sleep agent due to antihistiminic affect. (She could not get going until afternoon due to hangover effect). Went with Ambien CR. Treat anxiety as a symptom of depression by more aggressively treating the depression with “broad spectrum coverage”. Prozac targets Seratonin. Wellbutrin targets Dopamine and Strattera targets Norepnephrine. Or switching Prozac to Cymbalta with targets both Seratonin and Nor epinephrine. Then may consider adding a mood stabilizer.
- Apathetic Syndrome / Disorders of Diminished Motivation: akinetic mutism, abulia, apathy is a continuum of motivational loss This is very complicated topic. There are many factors that can influence motivation including medical states, emotional states, psychiatric states etc. It is important to consider the etiology of this syndrome to direct treatment planning efforts. The mechanism of motivation has been a topic of research. A model that has been proposed suggests a presence of a “core circuit” (Marin 1996b) that is a subsystem of the forebrain and includes anterior cingulum, nucleus accumbens, ventral pallidum and ventral tegmental area. The other limbic system structures amygdala, hippocampus, prefrontal cortex provides continuous modulation of the core circuit on the basis of motivational significance of the internal and external environment. Neurochemical mechanisms include the essential role of Dopamine systems in mediating responses to reward, novelty and elements of motivational behavior (McAllister 2000). Other biochemical changes include glutamate, acetylcholine etc. Conditions associated with DDM: Frontal Lobe damage Right Hemisphere Damage (right middle cerebral artery infarct) Cerebral White Matter (multiple sclerosis) Basal Ganglia (Parkinson’s Disease, Huntington’s Disease) Diencephalon: Wernicke – Korsakoff Syndrome Amygdala: Kluver – Bucy Syndrome Medical Disorders: hypothyroidism, Lyme Disease, Chronic Fatigue Syndrome Drug Induced: Neuroleptics, SSRI’s, chronic marijuana dependence Amphetimine or cocaine withdrawal Socio environmental: role change, institutionalism
- Pharmacology: Diagnose and treat conditions that may be contributing (hypothyroidism, parkinsons) Reduce or eliminate meds that may be negatively affecting motivation (Neuroleptics, SSRI’s) Treat depression in most effective manner Stimulants: Ritalin, etc Activating Antidepressants: Buspar, Parnate (MAO inhibitor), Dopamine Agonists: Amantadine, Bromocryptine, Levadopa Other psychotropics: Provigil, Aricept, Razadyne Environmental: set up the environment for optimum success. Set up for interaction, participation, stimulation and pleasure. Minimize social isolation, maximize lighting, orienting materials, consistency of approach, structured day, stimulating activities. Supportive Counseling / Therapies: counseling, supportive completion of ADL’s, physical activity that is goal directed, cognitive remediation (computer stimulation), recreational therapy Behavioral Interventions: functional trials to systematically determine client’s response to stimulation. Identify optimum environmental structure, time of day, reward preference, interaction style, prompt, etc.
- Early writings about head injury and resultant psychopathology (Adolf Meyer 1904 termed it “traumatic insanity”.
- Literature suggests that psychosis may follow a TBI months or years later. In one study (Buckley et al. 1993) in a series of case reports with patients with schizophrenia and premorbid TBI the onset of psychosis was 1, 9, 7, 16 and 11 years after the TBI occurred.
- Location of Injury: studies using CT scan evidence have shown left temporal and parietal regions (Sachdev et al. 2001). Primary sites of lesion are frontal and temporal cortices with secondary sites to be the hippocampus Severity of Injury: degree of severity is related to risk of posttraumatic psychosis. ie duration of unconsiousness, extent of damage on CT scan and degree of cognitive deficits. Recent study suggested that for patients with a family history of bipolar disorder or schizophrenia, risk of psychosis was unrelated to severity. Inherent Vulnerability to Psychosis: previous psychopatholigical disturbances have been reported in 83% or individuals who develop psychosis after TBI (Violon and De Mol 1987). Sachdev et al. 2001 reported that genetic vulnerability, having a first degree relative with a psychotic disorder, was found to be among the strongest predictors of who would develop psychosis following TBI. Gender: no clear role of gender in risk for PTP (selection of study, veterans, etc) IQ / Cognition: recent studies differ in findings (Fujii and Ahmed 2001) found no differences in IQ while Sachdev et al. 2001) found patients with PTP had more neurological deficits including lower IQ, worse verbal and non verbal memory, greater impairments in language. Socioeconomic Status: (Fujii and Ahmed 2001) found no differences in level of education Prior Neurological Disorder: (Fujii and Ahmed 2001) found significant more neurological pathology than in brain injured control groups including prior brain injury (14/25), siezures (3/25), learning disability (3/25), birth complications (2/25), ADHD (1/25) Post Traumatic Epilepsy: earlier studies suggested a that temporal lobe epilepsy greater risk for psychosis. More recent studies (2001) did not find a link between epilepsy and and post traumatic psychosis
- Pharmacology: side effects with Neuroleptics is tardive dyskinesia, sedation, extrapyramidal symptoms
- Findings: of the 445 clients with TBI, 6.5% were identified as having committed some form of sexual offense In all 128 individual offenses were committed. The most common was touching (combining Frotteurism and Toucherism) at 64.8%. Next was exhibitionism at 22.7% and overt sexual aggression at 9.4%. Only two clients had a prior history. The four main victim groups were staff, strangers, other people with TBI and family members. Staff members were twice as likely to be targets. Touching was the most common behavior exposed to staff. Children were victims in 15 of the 128 offenses (11.7%)