NeuroRehabilitation An Interdisciplinary Journal

ELSEVIER

NeuroRehabilitation 5 (1995) 245-254

Agitation in the older adult with traumatic brain injury David X. Cifu*, Jonathan C. Anderson, Eduardo Lopez Department of PM & R, Brain Injury Rehabilitation Programs, Rehabilitation and Research Center. Medical Col/ege of Virginia, Richmond, VA 23298-0661. USA Accepted 17 April 1995

Abstract Improvements in medical care and health have resulted in an increase in life expectancy and with it a steady increase in the number of older adults, which has resulted in an increasing number of brain-injured older adults. There is limited information available however, which specifically defines the incidence, management and outcome of behavioral sequelae, specifically agitation, in the older adult with TBI. The vast majority of the available literature addressing interventions in the agitated older adult, focuses on the individual with a psychiatric or dementing process who is a resident of a long-term care facility. Agitated behavior in the older adult with acute brain injury differs from this patient population and therefore management must also differ. Management includes behavioral strategies, environmental modifications, structured therapy sessions, appropriate medical management and neuropharmacologic interventions. There are no controlled studies which utilize standardized measures and examine the efficacy of these behavioral, environmental, therapeutical and pharmacological interventions for agitation in the older adult following TBI. In general, considerable care must be taken when using medications in the older adult. Alterations in absorption, pharmacokinetics, liver and renal metabolism, receptor sensitivity, side-effect tolerance, and compliance must all be considered. This article aims to present available information and provide a practical and clinically effective guide for the management of agitation in the older adult with brain injury.

Keywords: Agitation; Brain injury; Geriatric

1. Introduction

Traumatic brain injury (TBI) has been described as an epidemic in this country, with an

* Corresponding author, MCV Box 980661, Richmond, VA 23298-0661, USA.

estimated 0.5-1.5 million brain injured persons admitted to hospitals each year. These brain injuries occur in a bimodal age distribution, with the highest incidences in young (16-34 years) and older (65 years and older) adults. Improvements in medical care and health have resulted in an increase in life expectancy and with it a steady increase in the number of older adults, which has

1053-8135/95/$09.50 © 1995 Elsevier Science Ireland Ltd. All rights reserved. SSDII053-8135(95)00122-0

2411

DX Cifu et al. / NeuroRehabilitation 5 (1995) 245-254

resulted in an increasing number of brain injured older adults [1,2]. There has been a similar rise in the prevalence of ischemic and anoxic brain-injured older adults [3]. There is, however, a paucity of information available on the incidence, management and outcome of physical, behavioral and functional deficits which occur in this population. The formal and informal support systems available to assist in returning the brain-injured older adult to the community are limited, therefore it is vital that health care providers develop a better understanding of the appropriate management of the older adult with brain injury. One area of concern is the management of behavioral sequelae, in particular, agitation, in the brain-injured older adult. This article aims to present available information and provide a practical and clinically effective guide for the management of agitation in the older adult with brain injury. 2. Scope of the problem 2.1. Brain injury in the older adult It has been projected that the percentage of people over the age of 65 years will rise from its current level of 12% (25 million people), to 21 % (64 million) of the United States population by the year 2050. In addition, the oldest proportion of the population (aged 85 years and older) will increase from 1% (2 million) to nearly 5% (15 million) in that same time frame [1,2,4-8]. The

incidence of traumatic brain injuries in the geriatric population is not clearly defined, however, in those between 65 and 75 years of age, it is estimated at 200 in 100000 [9-13]. The overall gender distribution of TBI in the elderly is 1.4 males for every one female, although in the over age 80 subset, women predominate 3:2 [2,14-16]. Initial severity of brain injury appears to be unaffected by age [17]. Unlike younger age groups, the elderly sustain the majority of TBIs in domestic falls [14,16,18,19]. There are multiple risk factors for falls in the elderly, including generalized deconditioning, polypharmacy, osteoarthritis, hemiparesis, peripheral neuropathy, dementia and incontinence. Visual and auditory deficits, as well as

cerebellar and vestibular dysfunction may also contribute to falls. Hypotension or sedation due to specific medications can also predispose the elderly to falls [16,20]. These same risk factors for falls also predispose the elderly to motor vehicle, pedestrian and recreational accidents, all of which may result in traumatic brain injury [12,19,20]. Older adults are more likely to sustain focal cortical injuries and hematomas than younger adults, and are less likely to sustain diffuse axonal injury, largely due to differing mechanisms of injury [19,21-24]. Cerebral atrophy related to aging, increased fragility of vessel walls, and increased use of anti-clotting medications accounts for a higher frequency of subdural and subarachnoid hemorrhages, but an increased adherence of the dura to the skull from aging results in a lower frequency of epidural hemorrhage [22]. Older adults are more prone to secondary brain insult from hypoxia after a TBI, than are younger adults [3,25]. A decrease in 'cerebral reserve', related to the aging process, concomitant cerebral vascular disease, and alcohol use may complicate the pathophysiology of TBI in the older adult [17,26]. 2.2. Outcome in the older adult with brain injury

There are a number of investigations reported in the medical literature which examine the outcome of the older adult fOllowing TBI, primarily focusing on the positive association between increasing age and mortality [3,14,15,17,21,23]' There have been several retrospective studies examining the functional outcome of older adults who survive a traumatic brain injury. The majority show poorer prognosis for the older versus younger adult, with outcomes related to duration of coma, alcohol intake, general behavioral factors and social factors [2,19,22,26-29]. Specific behavioral factors, such as agitation, have not been directly linked with poor outcome in this age group. To the contrary, some studies have demonstrated that good outcomes are achievable in the older adult [2,14,16,30], and rehabilitation costs are similar between age groups [31]. None of these studies has addressed the impact of specific behaviors in this population.

D.x Cifu et al. / NeuroRehabilitation 5 (1995) 245-254

2.3. Agitation in brain injury Neuromedical issues following traumatic brain injury have been well identified, however, prospective investigations which clearly outline incidences, management strategies and outcomes have not been published. As a result of physiologic and pathologic changes which accompany aging, one would anticipate age-specific differences in the incidence and appropriate management of most common neuromedical complications after TBI [2,3,32]. Agitation has been defined in a variety of ways, depending on the presumed cause of the agitation and clinical background of the examiner. A critical review of the literature is limited by these differences in definition. The most practical definition of agitation after brain injury is any increase in psychomotor behavior which interferes with functional activities. The Agitated Behavior Scale [33] is the most useful tool to define and monitor agitation (see below). Restlessness or agitation following brain injury (traumatic, hypoxic or cerebrovascular) is not uncommon, and may become clinically significant in up to 50% of patients [34,35]. Restlessness has been considered a natural aftereffect of recovery from traumatic brain injury since the mid-1940s [36]. Agitation has been identified as a discrete stage in the Rancho Los Amigos levels of cognitive functioning (level IV) [37,38]. Some degree of agitation has been documented in onethird to one-half of TBI patients, and it often interferes with their participation in rehabilitation efforts [34,35]. Typically, it is brief in duration, from 1 to 14 days long, but in a small percentage of patients, it may last for an extended period of time. The etiology of the restless or agitated behavior may be related to focal areas of injury to the brain (e.g. temporal lobe epilepsy), but most commonly it is not clearly defined and may be due to a number of factors. Agitated TBI patients are more likely to require supervision after discharge, to require alternative institutional care and to have psychological adjustment difficulties [35]. There are a number of articles in the brain injury literature describing components of agitation [30,33,35,36,39-41], and a number of attempts to quantify these components [33,42,43].

247

There are no studies, however, which specifically define the incidence or outcome of agitation in the older adult with TBI. 3. Assessment of agitation The definition in the medical literature of agitation post-brain injury has been quite variable, which has resulted in discrepancies in incidence rates and efficacy of interventions. Clearly, the term 'agitation' cannot be defined as a single event or behavior, but rather a spectrum of behaviors. To quantify these behaviors, and to attempt to produce reproducible monitors of agitation, a number of agitation or aggression scales have been developed [33,34,43-46]. In general, these scales have been developed for cognitivelyimpaired individuals with aggressive behavior and have differed based on the cause of cognitive impairment (traumatic brain injury, Alzheimer's Disease, psychiatric disorders, vascular dementia). The scale specifically designed for the traumatically-injured older adult is the Agitated Behavior Scale (ABS), which includes the 14 behaviors most commonly associated with agitation ranked from 1 (absent) to 4 (present constantly) [33]. The scale is administered every 8 h by the treatment team, and has been standardized to rate agitation as; absent (14-20), mild agitation or restlessness (21-27), moderate (28-34) or severe (35 and above). Thus, any brain-injured individual scoring 21 or higher on the ABS may be defined as being 'agitated'. The every 8-h monitoring allows for the behaviors to be followed for diurnal and daily variations, as opposed to the more episodic monitoring, which tends to occur when extreme behaviors are noted. All older adults with acute brain injury should be monitored using the ABS for at least 72 h, once restless or agitated behavior is noted. Monitoring should be continued if a patient scores 21 or greater in 24 h, or if adjustments in treatment for behavior are being instituted. Some have advocated that, when used in concert with a structured, daily group orientation evaluation (Reality Orientation Group, Orientation Group Monitoring System), the ABS can assist in mea-

248

D.X Cifu et al. / NeuroRehabilitation 5 (1995) 245-254

suring behavioral effects of all medication, therapeutical, and environmental interventions [33,47]. 4. Management of agitation The central nervous system of the healthy older adult is highly sensitive to anything which affects its homeostasis, whether due to altered flow of cerebral spinal fluid, decreased oxygenation, central-acting medications, or excessive environmental stimuli. This is compounded in the face of acute brain injury. The level of arousal in the older adult with a brain injury may vary greatly, from comatose to agitated, depending on: the degree and type of injury, concomitant illness, pharmacologic agents, alcohol, secondary insults to the recovering brain, psychological factors, premorbid factors and environmental stimulation. The typical pattern of recovery includes initial diminished level of arousal, followed by some degree of hyperarousal and culminating in a return to a premorbid level of arousal. The treatment team can influence the safe and successful progression through these levels of arousal by limiting secondary insult, addressing concomitant illness, appropriately managing pharmacologic interventions and regulating environmental stimulation. The management of agitated behavior in the older adult with brain injury includes behavioral strategies [39,46,48,49], environmental modifications [29,48,50], structured therapy sessions [40,74], appropriate medical management and neuro-pharmacologic interventions [39,41,48,51-65]. The vast majority of the available literature addressing these interventions in the agitated older adult, focus on the individual with a dementing process who is a resident of a long-term care facility [66-74]. There are no controlled studies which utilize standardized measures and examine the efficacy of varying behavioral, environmental, therapeutical and pharmacological interventions for agitation following TBI. Additionally, there are no published investigations addressing the efficacy of any management options, specifically in the agitated older adult. Pharmacological management of agitation in the brain-injured adult has been well described, however, considerable variation exists

[39,41,48,51-65]. Use of psychopharmacologic

agents in the agitated (non-brain injured) older adult has also been well described [45,49,66,73,77-81]. While similarities may exist between these two populations, the brain-injured older adult should not necessarily be managed in the same manner as the older adult with agitation, due to psychiatric or dementing causes. In general, however, considerable care must be taken when using medications in the older adult. Alterations in absorption, pharmacokinetics, liver and renal metabolism, receptor sensitivity, side-effect tolerance, and compliance must all be considered. Typically, initiating any medication at low doses (often one-half of usual starting doses), and titrating, dosing slowly, is recommended. Additionally, it is important to have specific therapeutic goals and to re-evaluate the accomplishment of these goals frequently. Finally, when possible, use of a single agent is preferred, as polypharmacy may potentiate side effects. These dictums hold true for all pharmacologic interventions, but are crucial in the management of the brain-injured older adult. 4.1. Non-pharmacologic interventions

Limitations in health care resources have often necessitated early utilization of pharmacologic agents to rapidly manage agitated behavior in the older adult with brain injury. Ideally, nonpharmacologic agents should be implemented within the first 24 h after brain injury and, if possible, medications reserved for individuals refractory to this initial treatment [58]. Available medical literature in the area of non-pharmacologic management of agitation in the brain injured adult are predominantly anecdotal. Controlled trials with objective criteria for the monitoring of agitation are not currently available. The following are practical, largely non-pharmacologic management strategies for agitation in the brain-injured older adult, based on national trends and clinical experience. 4.1.1. Environmental

Regulating the amount and type of environmental stimuli must be part of every basic recov-

D.x Cifu et al. / NeuroRehabilitation 5 (1995) 245-254

ery program after brain injury. Additionally, limiting, unnecessary or inappropriate stimulation may prevent or decrease agitated behavior. Brain injury limits the ability to interpret stimuli and to filter out excess inputs. This is further compounded in the older adult, who often has a diminished acuity of the senses. Lighting should be adjusted to approximate day and night cycling. Daytime lighting should be maintained so as to prevent excessive shadows or glare. Auditory input (beeping of equipment, telephones, overhead speakers) should be minimized and limited to therapeutic interventions (neurologic checks, sensory stimulation, socialization, therapy sessions). Tactile input (needle sticks, foley catheters, nasogastric tubes, restraints, examinations) should be minimized and limited to therapeutic interventions as well.

4.1.2. Medical management A number of commonly used medications may have adverse central effects on the older adult with brain injury, which may potentiate agitation. These medications should be appropriately weaned as rapidly as possible. These include: central acting antihypertensives (beta-blockers, clonidine, aldomet), H2 blockers, metoclopramide, narcotic pain agents, benzodiazepines, steroids, theophylline and respiratory inhalers [3,82]. Common medical complications seen in the brain-injured older adult may also potentiate behavioral problems, including: infections (central nervous system, urinary tract, pulmonary), pain (musculoskeletal, distended bowel or bladder, cardiac, ileus), hypoxia, hydrocephalus, electrolyte abnormalities and psychiatric disorders. Monitoring for and treating these conditions will obviate more extensive behavioral interventions [83]. 4.1.3. Normalizing sleep-wake cycle Abnormalities in the sleep-wake cycle or sleep hygiene are common following acute brain injury, as well as with acute hospitalization for any reason. While environmental modifications (controlling auditory and visual stimuli) may correct some abnormalities, more often, difficulties remain. All brain-injured adults should have daily sleep-wake

249

charts maintained, and the have the goal of returning to premorbid sleep patterns within one week. In the older adult, scheduled rest periods are important (up-down schedules) and should be instituted on the first day of a program. While pharmacologic intervention is not preferred, it is typically necessary. Prompt use of an appropriate agent, and aggressive weaning of that agent once sleep hygiene is maintained is important. Trazodone is a highly effective and well tolerated agent in the older adult, including the very old. Other commonly used agents, such as diphenhydramine, chloral hydrate, tricyclic antidepressants and short-acting benzodiazepines, while effective as sleep agents, are not as well tolerated in the older adult Trazodone. Trazodone is a weak antidepressant agent, which also has a hypnotic effect, with minimal side effects on the brain-injured population. Its ability to increase circulating serotonin makes it useful as a nighttime sleep aide without potentially cognitively-impairing cholinergic side effects. It should be started initially at 50 mg, given at 8 or 9 p.m., and increased by 50 mg every 2 days, to a maximum single dosage of 300 mg, until the desired effect is achieved. The incidence of priapism and cardiac arrhythmias is rare, however, the clinician should be aware of these potential side effects [52,60,61,63].

4.1.4. Behavior modification As with any acute brain injured individual, the entire treatment team should consistently work on a program of behavior management, rewarding appropriate behaviors. Behavior modification may also be necessary to attempt to correct inappropriate behaviors, typically instituted by ignoring or negatively reinforcing these behaviors. These interventions may be difficult in the face of the cognitive and communication deficits which often accompany brain injury. Consistency among the treatment team, including the family, is vital. 4.1.5. Structured therapy sessions All interactions with an agitated, older brain-injured adult should be structured so as to include appropriate environmental controls, behavior management and modification, consideration of

250

D.X Cifu et aL / NeuroRehabilitation 5 (1995) 245-254

up-down schedules and extensive involvement of the family and other informal caregivers.

4.1.6. Physical restraints The use of another person or persons to prevent injury from agitated behaviors is preferable to physical restraints. Ideally, a familiar person (family or friend) could serve this role, however, usually, this is not practical. Professional staff are also usually unable to serve this need on a 24-h basis. Some have advocated the use of secured beds, which restrict agitated patients with netting or other obstacles [2,29]. Expense, inconvenience, risks of extremity compression injuries and strangulation, and a fear of acclimating the brain-injured individual to such a restricted environment, have limited their usage. When necessary to prevent injury to the patient or staff, judicious use of soft restraints (posey vests or extremity restraints) is an appropriate early intervention in the agitated older brain-injured adult. Restraints are often utilized until other first line agents have had time to work. Guidelines for the use of restraints and experiential protocols are replete in the medical literature [50,84,85]. Patients must never be ordered on an 'as needed basis', but rather for a specific observed behavior. Restraints must be monitored closely to prevent injury, and should be removed at least every 2 h to monitor skin integrity. Restrained individuals may be at increased risk for the development of venous thrombosis, thus appropriate prophylaxis (subcutaneous heparin 100 mg/kg every 12 h) is needed. Restraints should be discontinued as early as is feasible.

4.2. Pharmacologic interventions The available medical literature which examines the impact of pharmacologic agents on individuals with agitation is limited and predominantly anecdotal. A number of agents have been utilized, including propranolol, clonidine, buspirone, haloperidol, methylphenidate, amitriptyline, carbamazepine, lithium, trazodone and amantadine. There is little consistency in defining and quantifying agitation or improvement between studies. Additionally, none of the avail-

able studies employ a standardized measure of agitation [39,41,48,51-65]. As a result, pharmacologic guidelines based on scientific data are not available. The following is a practical guide to the use of neuropharmacologic agents to manage agitation in the older adult population, based on national trends and clinical experience.

4.2.1. First line agents Carbamazepine. The majority of patients who suffer a moderate to severe traumatic brain injury have an elevated seizure risk, which may warrant the use of an anticonvulsant agent for prophylaxis. Carbamazepine is an appropriate first line anticonvulsant in this patient population and, additionally, in the high therapeutic range, 8-12 mcg/ml, Carbamazepine is effective in controlling agitation. Carbamazepine acts as a 'membrane stabilizer', tending to prevent 'kindling' and rapid swings in behavior. The starting dose is 100 mg every 8 h, increasing by 100-300 mg every 2-3 days until the desired level is reached. Blood levels should be checked every 3 days, while adjusting dosages. Liver function studies and complete blood counts should be similarly checked, as hepatotoxicity and aplastic anemia are potential adverse reactions. Lethargy and cognitive impairment have been reported, but are typically limited to the initiation period (first week). Phenytoin and valproic acid may have similar anti-agitation effects, but they are not typically as effective [51,56,65,76,83]. Trazodone. As well as being a recommended hypnotic, a single nighttime dose of Trazodone may also improve day and nighttime agitation. Additionally, a 50-mg dose of Trazodone in the morning may assist with mild, persistent agitation. Unfortunately, sedation is a major side effect. Trazodone has also been advocated as an 'as needed' agitation medication (50 mg every 6 h), however, it may be too slow acting to be practical [52,60,61,63]. Lorazepam. Lorazepam is appropriate for short-term use on a 'as needed' basis (1-2 mg every 4 h p.o./i.m.) until other modalities take effect. It will cause sedation, and occasionally significant amnesia in the older adult, however, it is the best tolerated of the short-acting benzodi-

D.x Cifu et al. / NeuroRehabi/itation 5 (1995) 245-254

azepines. Lorazepam is preferred over Haloperidol, as it does not have some of the more serious side effects associated with neuroleptics, including potential exacerbation of agitation from diffuse axonal injury (DAn [51,56,65,76,86].

4.2.2. Second line agents Amantadine. Amantadine is a central-acting dopamine agonist, which has been advocated as an effective anti-agitation agent in the older adult. A second-line agent in the tr;~atment of Parkinsonism-induced rigidity and tremors, Amantadine has been used extensively in the older adult. It is given twice a day, initially in 50-mg doses and increased every 2-3 days by 100 mg, to a maximum of 400 mg/day. Doses greater than 300 mg/day have been suggested as potentiating risks of seizure. Amantadine may also precipitate psychosis in the older adult [51,53,56,65,76]. Amitriptyline. Amitriptyline is a tricyclic antidepressant, which, in doses less than 100 mg/day, has been advocated as an effective anti-agitation medication without significant cholinergic side effects. The small, but real risk of cardiac complications from Amitriptyline limits its use in the older adult. It is dosed similarly to Trazodone [41,51,56,59,65,76]. Haloperidol. Haloperidol is a rapidly acting neuroleptic, which works extremely effectively against agitation in the older adult. It is appropriate for short-term use only, secondary to cognitive and neuromuscular side effects associated with long-term usage. It may be given as a scheduled medication, until other agents have been initiated, or as an 'as needed' medication (0.5-2 mg p.o./i.m. every 4 h) for breakthrough agitation. It is especially effective on agitation associated with psychotic behavior and delirium in the older adult. Very low doses (0.25-0.5 mg) have been demonstrated to be effective in the older adult [51,56,65,76,87]. Propranolol. Propranolol is a centrally-acting l3-adrenergic antagonist, which has proven useful in episodic severe agitation. It is initiated at 20 mg three times a day, and increased by 20-60 mg every 2-3 days, with close monitoring of blood pressure. Use of the long-acting formulation is preferred to prevent an on/off phenomenon.

251

Propranolol can be rapidly (20-60 mg daily) weaned off once agitation is controlled, with rare recurrence of behaviors. Hypotension and bradycardia limit dosing in the older adult [51,54-56,65,76]. Buspirone. Buspirone is a serotoninergic anxiolytic agent, which does not have the significant side effects of the benzodiazepines. It may have some effect on mild agitation (restlessness) and anxiety, but typically takes from 1 to 2 weeks to have effect, and therefore is of limited use in acute agitation. Thus, although a safe medication in the older adult, it is reserved for the anxious patient. Dosing begins at 10 mg a day, in two doses, and increases to 30-45 mg a day, in three doses, after 1-2 weeks. Transient headaches and dizziness are often associated with initial use [51,56,57,65,76].

4.2.3. Third line agents Bromocriptine. Bromocriptine is a dopamine agonist, which is used as an adjunctive treatment for Parkinson's Disease. It may have some effect on mild to moderate agitation, perhaps by improving attention. It is typically well tolerated in the older adult, dosed initially at 2.5-5.0 mg/day in divided doses, and increased by 5.0 mg/week, to a maximum dose of 15.0 mg/day [51,56,65,76]. Nifedipine. Nifedipine and the other caIciumchannel blockers have been shown to have some effect on agitation, with hypotension being the limiting side effect. The long-acting formulation is preferable to prevent fluctuations in blood levels and an on/off phenomenon. Propranolol appears to have more consistent efficacy [51,56,65,76]. Clonidine. Clonidine has been reported to be effective for agitation, with hypotension and sedation being the limiting side effects in the older adult. Dosing begins at 0.1 mg one to three times a day, and increases by 0.3 mg every 2-3 days. The sustained-release transdermal patch will prevent an on/off phenomenon [51,56,65,75,76]. Lithium. Lithium is very effective in preventing rapid swings in behavior, similar to its effects on mania. Nausea, emesis and diarrhea are its major limiting side effects, however, in the elderly, sedation may also occur. Caution must be used with

252

D.x Cifu et al. / NeuroRehabilitation 5 (1995) 245-254

this agent, particularly in the older adult, as it has a narrow therapeutic window, as well as a small therapeutic index [51,56,65,76]. 5. Summary

[11]

[12] [13]

The increasing incidence and prevalence of older adults with traumatic brain injury, necessitates a better understanding of the management of neuromedical sequelae seen in this patient population. Agitation is a common behavior seen after brain injury and one which requires a specialized approach to treatment in the older adult. A comprehensive approach utilizing environmental controls, appropriate medical management, normalization of sleep/wake cycles, behavior management, structured therapy sessions and judicious use of physical restraints and psychopharmacology is vital. Further investigations exploring the efficacy of these interventions are also important.

[19]

References

[20]

[1] Cifu DX. Rehabilitation of the elderly crash victim. Clin Geriatr Med 1993;9:473-483. [2] Goodman H, Englander J. Traumatic brain injury in elderly individuals. Phys Med Rehabil Clin 1992;3:441-459. [3] Cifu DX, Means KM, Currie DM, Gershkoff AM. Geriatric rehabilitation: Diagnosis and management of acquired disabling disorders. Arch Phys Med Rehabil 1993;74:S406-S412. [4] American Medical Association. White paper on elderly health. Arch Int Med 1990;150:2459-2472. [5] Brotman HB. Every ninth American: An analysis for the Chairman of the Select Committee on Aging, House of Representatives. Comm Pub No 97-332. Washington, DC, US Government Printing Office, 1982. [6] Clark GS, Murray PK. Rehabilitation of the geriatric patient. In: Delisa JA, ed. Rehabilitation Medicine. Philadelphia: JB Lippincott, 1988;10. [7] Taeuber CM. America in transition. An aging society. Current Population Reports, Series P-23, No. 128. Washington, DC, Bureau of the Census, 1983. [8] US Senate Special Committee on Aging. Developments in Aging. Washington, DC, 1988;1:2. [9] Frankowski RF. Descriptive epidemiologic studies of head injury in the United States: 1974-1984. Adv Psychosom Med 1986;16:153-172. [10] Frankowski RF, Annegers JF, Whitman S. Epidemiologic and descriptive studies, Part I. The descriptive

[21]

[14] [15]

[16] [17]

[18]

[22] [23] [24]

[25] [26]

[27] [28] [29]

[30] [31]

epidemiology of head trauma in the U.S. C.N.S. Trauma Status Report 1985;109:33-43. Klauber MR, Marshall LF et al. Prospective study of patients hospitalized in San Diego County, 1978. Neurosurgery 1981;9:236-24l. Kraus JF. Injury to the head and spinal cord. J Neurosurg 1980;53:S3-S1O. Kraus JF, Black MA et al. The incidence of acute brain injury and serious impairment in a defined population. Am J Epidemiol 1983;119:186-20l. Amacher AL, Bybee DE. Toleration of head injury by the elderly. Neurosurgery 1979;20:954-957. Sosin DN, Sacks 11, Smith SM. Head injury-associated deaths in the U.S. from 1979 to 1986. JAmMed Assoc 1989;282:2251-2258. Wilson JA. The functional effects of head injury in the elderly. Brain Inj 1987;1:183-188. Miller JD, Jones PA. Minor head injury. In: Rosenthal M, Griffith E, Bond M and Miller JD, eds. Rehabilitation of the Adult and Child With Traumatic Brain Injury. Philadelphia: FA Davis, 1990;236-246. Hom U, Cope DN. Demographics. In: Hom U and Cope ND, eds. Traumatic Brain Injury. Philadelphia: Hanley and Belfus, 1989;X. Katz DI, Kehs GJ, Alexander MD. Prognosis and recovery from TBI: The influence of advancing age. Neurology 1990;40:276. Lehman LB. Head trauma in the elderly. Postgrad Geriatr 1988;83:140-147. Heiskanen H, Sipponen P. Prognosis of severe brain injury. Acta Neurol Scand 1970;46:343-348. Herneasniemi J. Outcome following head injuries in the aged. Acta Neurochir 1979;49:67-79. Jennett B, Teasdal G et al. Predicting outcome in individual patients after severe head injury. Lancet 1976;1031-1034. Kalsbeek WB, McLaurin RL et al. The national head and spinal cord injury survey. Major findings. J Neurosurg 1980;53:S19-S3l. Brandstater ME. Unique aspects of rehabilitating the elderly with head injury. Am Acad Phys Med Rehabil Proc 1990;1:26-29. Galbraith S, Murray WR et al. The relationship between alcohol and head injury and its effects on the conscious level. Br J Surg 1976;63:128-130. Carlsson CA, von Essen C, Losgren J. Clinical factors in severe head injuries. J Neurosurg 1968;29:242-251. Galbraith S. Head injuries in the elderly. Br Med J 1987;294:294-325. Williams LM, Morton GA, Patrick CH. The Emory cubicle bed. An alternative to restraints for agitated traumatically brain-injured clients. Rehabil Nurs 1990;15:1,30-33. Levati A, Farina M et al. Prognosis of severe head injuries. J Neurosurg 1982;57:779-783. Saywell RM, Woods JR, Rappaport SA, Allen TL. The value of age and severity as predictors of costs in geri-

D.x Cifu et al. / NeuroRehabilitation 5 (1995) 245-254

[32] [33] [34] [35]

[36] [37]

[38]

[39]

[40] [41] [42]

[43] [44] [45]

[46] [47]

[48]

atric head injury trauma patients. J Am Geriatr Soc 1989;37:625-630. Gershkoff AM, Cifu DX, Means KM. Geriatric rehabilitation. Social, attitudinal and economic factors. Arch Phys Med Rehabil 1993;74:S402-S405. Corrigan JD. Development of a scale for assessment of agitation following traumatic brain injury. J Clin Exp Neuropsychol 1989;11:261-277. Levin HS, Grossmean RG. Behavioural sequelae of closed head injury: Quantitative study. Arch Neurol 1978;35:720-727. Reyes RL, Bhattacharyya AK, Heier D. Traumatic head injury: Restlessness and agitation as prognosticators of physical and psychological improvements in patients. Arch Phys Med Rehabil 1981;62:20-23. Denny-Brown D. Disability arising from closed head injury. JAmMed Assoc 1945;127:429-436. Corrigan JD, Mysiw WJ. Agitation following traumatic brain injury: Equivocal evidence for a discrete stage of cognitive recovery. Arch Phys Med Rehabil 1988;69:487-492. Malkmus D, Booth BJ, Kodimer C. Rehabilitation of the Head-Injured Adult. Comprehensive Cognitive Management. Downey, CA, Professional Staff Association of Rancho Los Amigos Hospital, Inc. 1980; Brooke MM, Questrad KA, Patterson DR, Bashak KJ. Agitation and restlessness after closed head injury. A prospective study of 100 consecutive admissions. Arch Phys Med RehabilI992;73:320-323. Fauman MA. Treatment of the agitated patient with an organic brain disorder. J Am Med Assoc 1978;240:380-382. Jackson RD, Corrigan JD, Arnett JA. Amitriptyline for agitation in head injury. Arch Phys Med Rehabil 1985;66:180-181. Levin HS, High WM et al. The Neurobehavioral Rating Scale: Assessment of the behavioral sequelae of head injury by the clinician. J Neurol Neurosurg Psychiatry 1987;50:183-193. Silver JM, Yudofsky SC. The Overt Aggression Scale. Overview and guiding principles. J Neuropsychiatry 1991;3:S22-S29. Gercher LA, Buckwatter KC. A nursing challenge. A~­ sessment and management of agitation in Alzheimer's patients. J Gerontol Nurs 1994;20:11-20. Sultzer DL, Levin HS et al. Assessment of cognitive, psychiatric and behavioral disturbances in patients with dementia. The Neurobehavioral Rating Scale. J Am Geriatr Soc 1992;40:549-555. Tesar GE. The agitated patient, Part I. Evaluation and behavioral management. Hosp Comm Psychiatry 1993;44:329-331. Corrigan JD, Arnett JA, Houck U, Jackson RD. Reality orientation for brain-injured patients. Group treatment and monitoring of recovery. Arch Phys Med Rehabil 1985;66:626-630. Herbel K, Schermerhorn L, Howard J. Management of

[49] [50] [51] [52]

[53] [54] [55] [56] [57] [58] [59] [60] [61] [62] [63] [64]

[65] [66]

253

agitated head-injured patients. A survey of current techniques. Rehabil Nurs 1990;15:66-69. Patten TS, Sayert M. Behavioral management of the agitated head trauma client. Rehabil Nurs 1990;15:248-249. Edlund MJ, Goldberg RJ, Morris pc. The use of physical restraints in patients with cerebral contusion. Int J Psychiatry Med 1991;21:173-182. Cardenas DD, McLean A. Psychopharmacologic management of traumatic brain injury. Phys Med Rehabil Clin 1992;3:273-290. Cassidy JW. Pharmacological treatment of posttraumatic behavioral disorders. Aggression and disorders of mood. In: Wood RLI, ed. Neuro-Behavioral Sequelae of Traumatic Brain Injury. London: Lawrence Erlbaum, 1990;219-247. Chandler MC, Barnhill JB, Gaultieri CT. Amantadine for the agitated head-injury patient. Brain Inj 1988;2:309-311. Elliot FA. Propranolol for the control of the belligerent behavior following acute brain damage. Ann Neurol 1977;1:489-491. Greendyke RM, Kanter DR et al. Propranolol treatment of assaultive patients with organic brain disease. J Nerv Ment Dis 1986;174:290-294. Gualtieri CT. Psychopharmacology of traumatic brain injury. In: Neuropsychiatry and Behavioral Pharmacology. New York: Springer-Verlag, 1991;37-88. Levine AM. Case report. Buspirone and agitation in head injury. Brain Inj 1988;2:165-167. Ludwig BL Conference summary. Psychopharmacological management of the difficult patient. J Neurol Rehabil 1989;3:147-149. Mysiw WJ, Jackson RD, Corrigan JD. Amitryptaline for posttraumatic agitation. Am J Phys Med Rehabil 1988;67:29-33. Pinner E, Rich CL. Effects of trazodone on aggressive behavior in seven patients with organic mental disorders. Am J Psychiatry 1988;145:1295-6. O'Shanick GJ. Closed head injury. In: Michels R, Cavenar JO, Cooper AM, et aI., eds. Psychiatry. Philadelphia: JB Lippincott. 1988. Ratey JJ, Gordon A. The psychopharmacology of aggression. Toward a new day. Psychopharmacol Bull 1993;29:65-73. Simpson DM, Foster D. Improvement in organically disturbed behavior with trazodone treatment. J Clin Psychiatry 1986;47:191-3. Van Woerkem T, Teelken A, Minderhoud J. Difference in neurotransmitter metabolism in frontotemporal lobe contusion and diffuse cerebral contusion. Lancet 1977;i:812-813. Zasler ND. Review. Advances in neuropharmacological rehabilitation for brain dysfunction. Brain Inj 1992;6:1-14. Aless CA. Managing behavioral problems of dementia in the home. Clin Geriatr Med 1991;7:787-801.

254

DX cifu et al. / NeuroRehabilitation 5 (1995) 245-254

[67] Beck C, Rossby L, Baldwin B. Correlates of disruptive behavior in cognitively-impaired elderly nursing home residents. Arch Psychiatr Nurs 1991;5:281-29l. [68] Chrisman M, Tabar D, Whall AL, Booth DE. Agitated behavior in the cognitively-impaired elderly. J Gerontol Nurs 1991;17:9-13. [69] Cohen-Mansfield J. Agitation in the elderly. Adv Psychosom Med 1989;19:101-113. [70] Cohen-Mansfield J, Marx MS, Werner P. Agitation in elderly persons: An integrative report of findings in a nursing home. Int Psychogeriatr 1992;4:221-240. [71] Colonda CC, Hamer RM. Antecedents and interventions for aggressive behavior of patients at a geropsychiatric state hospital. Hosp Comm Psychiatry 1991;42:287-292. [72] Goddauer J, Abraham IL. Effects of relaxing music on agitation during meals among nursing home residents with severe cognitive impairment. Arch Psychiatr Nurs 1994;8:150-158. [73] Kolcaba K, Miller LA. Geropharmacology treatment. Behavioral problems extend nursing responsibility. J Gerontol Nurs 1989;15:29-35. [74] Schneider LS, Sobin PB. Non-neuroleptic treatment of behavioral symptoms and agitation in Alzheimer's Disease and other dementia. Psychopharmacol Bull 1992;28:71-79. [75] Bakchine S, Lacomblez et al. Manic-like state after bilateral orbitofrontal and right temporoparietal injury. Efficacy of c1onidine. Neurology 1989;39:777-78l. [76] Tesar GE. The agitated patient, Part II. Pharmacologic treatment. Hosp Comm Psychiatry 1993;44:627-629.

[77] Billig N, Cohen-Mansfield L, Lipson S. Pharmacological treatment of agitation in a nursing home. J Am Geriatr Soc 1991;39:1002-1005. [78] Kunik ME, Yudofsky SC, Silver JM, Hales RE. Pharmacologic approach to management of agitation associated with dementia. J Clin Psychiatry 1994;55S:13-17. [79] Pollock BG, Perel JM, Reynolds CF. Pharmacodynamic issues relevant to geriatric psychopharmacology. J Geriatr Psychiatry NeuroI1990;3:221-228. [80] Rosen J, Bohon S, Gershon S. Antipsychotics in the elderly. Acta Psychiatr Scand SuppI1990;358:170-175. [81] Sinnet PF. Restless patients in nursing homes. What is the role of drug therapy? Drugs Aging 1994;4:443-448. [82] Schroeder JA, Wolfe WM et al. The effect of intravenous ranitidine and metoclopramide on behavior, cognitive function and affect. Anesth Analg 1994;78:359-364. [83] Slagle DA. Psychiatric disorders following closed head injury. An overview of biopsychosocial factors in their etiology and management. Int J Psychiatr Med 1990;20: 1-35. [84] Brungardt GS. Patient restraints. New guidelines for a less restrictive approach. Geriatrics 1994;49:43-44. [85] Marks W. Physical restraints in the practice of medicine. Current concepts. Arch Intern Med 1992;152:2203-2206. [86] Ancill RJ, Carlyle WW, Liang RA, Hollidey SG. Agitation in the demented elderly. A role for benzodiazepines? Int Clin Psychopharmacol 1991;6:141-146. [87] Schneider LS, Pollock YE, Lyness SA A meta-analysis of controlled trials of neuroleptic treatment in dementia. J Am Geriatr Soc 1990;38:553-563.

Agitation in the older adult with traumatic brain injury.

Improvements in medical care and health have resulted in an increase in life expectancy and with it a steady increase in the number of older adults, w...
2MB Sizes 2 Downloads 0 Views