Cognitive-behavioral recovery in comatose patients following auditory sensory stimulation.
(Care and treatment)
Davis, Alice E.
|Publication:||Name: Journal of Neuroscience Nursing Publisher: American Association of Neuroscience Nurses Audience: Professional Format: Magazine/Journal Subject: Health care industry Copyright: COPYRIGHT 2003 American Association of Neuroscience Nurses ISSN: 0888-0395|
|Issue:||Date: August, 2003 Source Volume: 35 Source Issue: 4|
|Topic:||Event Code: 310 Science & research|
|Geographic:||Geographic Scope: United States Geographic Code: 1USA United States|
Abstract: Nursing therapies promote recovery following severe
traumatic brain injury (TBI). However, the type and dose of treatment
needed to stimulate functional plasticity have not been determined. In
this quasi-experimental study, the effects of a structured auditory
sensory stimulation program (SSP) were examined in 12 male patients,
17-55 years old, with severe TBI. SSP was initiated 3 days after injury
and continued for 7 days. Recovery was measured by comparing baseline
Glasgow Coma Scale (GCS), Sensory Stimulation Assessment Measure (SSAM),
Ranchos Los Amigos Level of Cognitive Functioning Scale (RLA), and
Disability Rating Scale (DRS) scores to ending scores between those who
received SSP and those who did not. For the intervention group a
positive recovery of function trajectory was found for mean GCS, and
there was a greater improvement in GCS and RLA scores between baseline
and discharge testing periods. DRS and SSAM scores at baseline and at
discharge were significantly different. SSP did not affect hemodynamic
or cerebral dynamic status. Early and repeated exposure to an SSP may
promote arousal from severe TBI without adversely influencing cerebral
Traumatic brain injury (TBI) occurs in approximately 1.5 million-2 million people each year in the United States, accounting for more than 500,000 hospitalizations. Although emergency care, diagnostic technology, medical intervention, and nursing care have resulted in increased survival following TBI, arousal and cognitive recovery are not guaranteed. More than 90,000 of those persons who are hospitalized with TBI suffer injuries of such magnitude that long-term cognitive, behavioral, and emotional impairments prevent them from pursuing active and responsible lives after injury (National Institutes of Health [NIH] Consensus Development Panel, 1999).
Cope and Hall (1982) determined that early rehabilitation after brain injury produced better outcomes. With the current state of knowledge related to activation of recovery mechanisms immediately following brain injury, it can be argued that early environmental stimuli via a sensory stimulation program may enhance recovery processes such as plasticity, which is demonstrated as increased arousal in comatose patients. The purpose of this study was to examine behavioral effects of a structured sensory stimulation program (SSP) on arousal in patients with TBI who were in coma. The specific research questions addressed were (a) Will there be an increase in arousal between initial assessment (baseline) and discharge assessment scores as measured by the Glasgow Coma Scale (GCS), Sensory Stimulation Assessment Measure (SSAM), Ranchos Los Amigos Level of Cognitive Functioning Scale (RLA), and Disability Rating Scale (DRS) in patients who receive an auditory sensory stimulation program? and (b) What is the effect of an auditory sensory stimulation program on cerebral hemodynamic status (intracranial pressure) [ICP]) and cardiopulmonary status (i.e., heart rate [HR], respiratory rate [RR], and mean arterial pressure [MAP])?
A profound sequelae of severe TBI, coma is often seen in critically ill brain-injured patients. Coma is defined as an unarousable, unresponsive state without eye opening, verbalization, or ability to follow commands (Jennett & Teasdale, 1981; Plum & Posner, 1980). Coma occurs from a variety of local or diffuse injuries that disrupt the reticular activating system (RAS) of the brainstem. Arousal, the foundational element of information processing, is maintained by the RAS. Arousal is a prerequisite for the selective attention necessary for recognizing and processing information. Without arousal, more complex cognitive processes, such as sustained attention or concentration necessary for learning, cannot occur (Arciniegas et al., 1999). Coma of any duration disrupts arousal mechanisms and interferes with the person's ability to respond to environmental stimuli. Coma of increased duration (>24 hours) has been linked to poor recovery and impaired functional outcomes (Gennarelli, et al. 1982).
Brain injury, although initiated at the moment of impact, is a process that evolves over hours and weeks (Gennarelli, 1997; Povlishock & Christman, 1995). Moreover, there is a growing body of knowledge from the fields of medicine, psychology, and neuroscience that recovery processes are activated immediately following TBI (McIntosh, Juhler, & Weiloch, 1998). One such recovery process, plasticity, allows the mature brain to modify its organization and function (Bach-y-Rita, 1990). Evidence of plasticity has been noted throughout the nervous system and includes neurochemical, receptor, and structural changes. Changes related to plasticity appear as dendritic branching, an increase in the number of receptor sites, changes in the configuration of synapses, and formation of new synapses (i.e., synaptogenesis; Kolb & Gibb, 1991; Stein, 1994).
Enhancement of plasticity is known to occur through both endogenous factors, such as the release of nerve growth factor (McDermott et al., 1997; McIntosh et al., 1998), and exogenous factors, such as environmental stimulation. The use of environment to enhance plasticity and improve neurological function has been extensively studied in animal models of injury and ischemia (Dalrymple-Alford & Kelche 1985; Galani, Jarrard, Will, & Kelche, 1997).
The direct effect of environment on plasticity in human studies is more difficult to determine. There is substantial but indirect evidence that environmental stimulation can be used in an intervention to improve cognitive function and produce behavioral change in humans. One such clinical intervention, sensory stimulation, uses environmental stimuli as a means to improve arousal in comatose, brain-injured patients. The clinical use of stimulation programs with comatose patients has garnered some success (Kater, 1989; LeWinn & Dimancescu, 1978; Mackay, Berstein, Chapman, Morgan, & Milazzo, 1992; Mitchell, Bradley, Welch, & Britton, 1990; Radar, Alston, & Ellis, 1989; Wilson, Powell, Elliots, & Thwaites, 1991). Although reported improvements in arousal following the implementation of a sensory stimulation program are pro,sing, the scientific methods and procedures have differed so significantly from study to study that interpretation and generalization of results are difficult.
Sensory stimulation has also been examined for its effects on cerebral dynamics. The use of auditory stimulation as a single stimulation modality has been studied with respect to its effects on ICP and cerebral perfusion pressure (CPP). The effect of auditory stimuli on ICP and CPP, using a variety of auditory configurations including familiar and unfamiliar voices, music, and environmental noise, has yielded controversial results. Mitchell and Mauss (1978) described increases in ventricular fluid drainage with patients who were exposed to conversations related to their condition but little change in drainage during routine conversation. Snyder (1983) described changes in ICP during conversations about the patient; however, other nursing care activities were occurring simultaneously. Consequently the actual effect of conversation was difficult to determine. In contrast, Prins (1989) found there was no significant effect on ICP with verbal and tactile interactions of family members. The work of Trealor, Nalli Guin, and Gary (1991) suggested that neither familiar nor unfamiliar voices significantly change ICP. Johnson, Omery, and Nikas (1989) documented no significant change in ICP during emotionally referenced conversation but found a significant decrease in ICP during times when conversation was unrelated to the patient. Schinner et al. (1995) demonstrated no significant effects on ICP and CPP during three types of auditory stimuli including music, environmental noise from the intensive care unit, and use of earplugs. Sisson (1990) examined behavioral and electroencephalogram (EEG) changes with auditory stimulation in brain-injured patients with GCS scores between 4 and 8. The study reported behavioral changes such as eye opening and extremity movement as well as EEG changes. However, these changes were not consistent across patients. Overall, these studies indicate that auditory stimuli may not be a significant factor in ICP and CPP changes. These results are based on the assumption that hearing pathways are intact following severe traumatic injury.
Design and Sample
Before data collection was initiated, this study was reviewed and approved by the institutional review boards at the medical centers where the study was conducted. A repeated measures pre- and posttest design with an intervention and control group was used for this study. In this quasi-experimental study, a purposive sampling technique was used. Participants were selected based on the specific criteria discussed below and purposively assigned to the intervention or control group.
Males were chosen for this study because they represent the group most likely to sustain a brain injury. The age range, 17-55 years, represents an age range documented to experience traumatic injury (Baker, O'Neill, & Haddon, 1974). Intervention participants were enrolled first, followed by control group participants. This approach was taken, rather than random assignment, to eliminate perceived differences in care between groups by family members who potentially used the same waiting room and often shared stories.
Participants were enrolled in the study a minimum of 3 days after sustaining brain injury if they had a GCS score of [less than or equal to] 8 (Teasdale, & Jennett, 1974) and had stable ICE which was defined as [less than or equal to] 20 mm Hg for 24 hours prior to entry into the study. An RLA score (Malkamus, Booth, & Kodimer, 1980) between Level I and Level III, which identified them as being either unresponsive to sensory stimuli or responding at a low or inconsistent level to sensory stimuli, was required.
Brainstem auditory evoked responses (BAERs) and EEGs were obtained prior to commencement of stimulation and at the end of the study. BAER was required to document that auditory pathways were intact. The pre-and postintervention EEGs were used to examine changes in electrical responses from baseline (i.e., the time participant was enrolled) to completion of the study. The BAERs and EEGs were performed by a trained EEG technician following the guidelines of the respective neurology departments. An attending neurologist interpreted all BAER and EEG results. Only patients with normal BAERs were enrolled in the study.
Once participants were identified as potential candidates for the study, they were followed daily until they met the clinical parameters for enrollment (i.e., 72 hours after injury and stable ICP for [less than or equal to] 24 hours). Family members were approached for consent when the participant met the clinical criteria for eligibility. BAERs and EEGs were performed after informed consent was obtained.
Variables and Measures
Change in arousal, the primary dependent variable, was measured by using standard clinical markers indicative of improvement in (a) level of coma (GCS), (b) response to sensory stimulation (SAM; Radar et al., 1989), (c) cognition (RLA), and (d) functional ability (DRS; Rappaport, Hall, Hopkins, Belleza, & Cope, 1982).
GCS is a composite score used to assess neurological function and level of arousal (Teasdale & Jenett, 1974). GCS is based on the numerical value assigned to an individual's best eye opening, verbal, and motor responses. Each response is scored separately and then totaled. Scores range from 3 to 15, with 3 indicating severe neurological deficits (i.e., severe coma) and 15 representing no deficits (i.e., awake, alert, and oriented). Interrater reliability using the Pearson's r = 0.95 and Cronbach's alpha 0.069 (p < .0001) has been reported (Segatore & Way, 1992). An increase in baseline and discharge scores represented a change in arousal.
Ranchos Los Amigos Level of Cognitive Functioning Scale. RLA (Malkamus et al., 1980) is an eight-level behavioral rating scale used to evaluate cognitive function based on behavioral responses to patients with varying stages of arousal. The scale represents the progression of recovery of cognitive structures as demonstrated through behavioral change. The RLA score is recommended for use in determining level of function within normally and random fluctuating environments and within structured settings where environmental stimuli are purposefully manipulated (Malkamus et al.). A high degree of interrater reliability has been documented using this instrument. For the purposes of this study, an increase in RLA score between baseline and discharge represented a change in arousal.
Disability Rating Scale. DRS (Rappaport et al., 1982) is a six-category functional outcome measure used to determine brain injury recovery. Scores range from 0 (complete recovery) to 30 (death). Reliability and validity have been established (Rappaport et al.). A decrease in score between baseline and discharge scores represented a change in arousal.
Sensory Stimulation Assessment Measure. SSAM (Radar et al., 1989) is an objective measure of the responsiveness of brain-injured patients between RLA I and IV. Stimuli are presented to five senses, and best response is measured using a sensory stimulation response scale (SSRS). SSRS measures the intensity of the responses to stimuli within three categories: eye opening, motor, and vocalization. In each of the three categories, six behavioral response choices can be selected, ranging from no response to able to follow commands or communicate ideas. Scores in each of the three categories are summed (range 3-36) to determine a response score. A general responsiveness score is calculated by summing the scores from each of the five senses. Test-retest reliability of the scale was 0.93 with an interrater reliability of 0.89. Concurrent validity of SSAM as a measure of sensory responsiveness was established using RLA, GCS, and DRS. Responses to stimuli were recorded using a modification of the grading scale developed by Radar et al. (1989), which provided a 6-point scale for best verbal, motor, and eye responses. SSRS scores were obtained for all categories during all stimulation sessions (up to eight times/day), allowing for calculation of individual responsiveness to each stimuli by time, day, and across time.
Injury Severity Score. ISS is a calculated score of injury based on the site and severity of anatomical injury (Baker et al., 1974). Scores range from 1 to 75, with scores of 15 or greater considered severe injury.
Postinjury day and admission to the study. Postinjury day (PID) begins with admission to the hospital. Admission to the study was based on ICP; an ICP < 20 mm Hg for 24 hours after the third PID was required.
To ensure safety and to prevent untoward effects in this critically ill sample, the study protocol included monitoring of clinical parameters: MAP, ICP, CPP, HR, and RR. Clinical parameters were recorded before and after each intervention. Demographic features of the sample also were collected: age, mechanism of injury, hospital discharge disposition, type of brain injury, and other anatomical injuries. An ISS was calculated to determine the overall magnitude of the traumatic injury. PIDs, beginning with day of injury through completion of the study, were tracked for all participants.
The independent variable was a unimodal (auditory only) sensory stimulation intervention. The categories of auditory stimulation varied and represented a wide range of tone frequencies (e.g., claps, bells, and music), diverse voice patterns (familiar and unfamiliar), and messages requiring simple (orientation phrases) to complex interpretative processes (commands). Families and friends of patients in the intervention group were encouraged to participate; their interactions served as familiar voices. They were guided in recording a personal family message that was used during those times when they were not present to interact with the patient.
For the intervention group the type and duration of the stimuli stayed constant, but the sequence of delivery and the number of stimulation sessions varied daily based on visitation time of family and friends, participant involvement in procedures and diagnostic tests, and physiologic stability (Table 1). All auditory stimuli (e.g., claps and bells, music, familiar voices, orientation and command phrases, and radio or television) were provided at least once each day, but the session time was randomly assigned.
After participants were identified as potential candidates for the study, they were followed daily until they met the clinical parameters for enrollment. Family members were approached for consent when the participant met the clinical criteria for eligibility. BAERs and EEGs were performed after informed consent was obtained. For all participants, arousal, cognitive, behavioral, and outcome measures were recorded at the beginning of the study and at the completion of the study. Participants in both the intervention and control groups received routine nursing care and rehabilitation services consistent with the standard of care for TBI patients provided in the hospital. Procedures for the intervention and control groups were as follows.
The structure of the intervention program was similar for all participants. Stimuli were delivered each day for up to 7 days. Participants received 5-8 stimulation sessions per day (between 8 am and 5 pm). Daylight hours were chosen to keep stimuli (aimed at arousal) consistent with normal waking hours. The minimal interval between sessions was 1 hour and a session duration was 5-15 minutes, depending upon the type of stimuli (Table 1). Prior to and following each stimulation session, the clinical parameters (i.e., MAP, ICE CPP, HR, and RR), the arousal measures (i.e., GCS score and RLA level), and the behavioral responses (i.e., SSAM) were recorded. SSP was discontinued if the patient began to follow commands or demonstrated cognitive change beyond a RLA Level III. SSP was postponed if dire medical complications arose and restarted after the medical emergency had been resolved. For the control group, only hourly GCS and RLA scores were collected.
Change in arousal, the primary dependent variable, was analyzed based on numerical change in GCS score, SSAM, RLA, and DRS scores. Changes in the SSAM, RLA, and DRS scores (i.e., difference between baseline and termination of study scores) were calculated and analyzed by using the Student's t test. Daily mean GCS scores were calculated for each group, analyzed across time using repeated measures analysis of variance, and compared for changes.
For the intervention group, the effect of stimulation, measured by eye/motor responses, was evaluated over time based on PID, stimulation type (e.g., family, music, orientation), and PID by stimulation type. The effect of stimulation on clinical variables including ICP, HR, RR, and MAP were analyzed over time to determine interactions by PID, stimulation type, and PID by stimulation type.
Twelve male patients hospitalized for severe TBI were enrolled in the study and assigned to either the intervention (n = 9) or control (n = 3) groups. Patients suffered closed head injuries of all types (Table 2). The patients ranged in age from 17 to 55 years. The sample was not statistically different between groups for age, injury severity score, and baseline GCS Score (Table 3). Motor vehicle collision was the most frequent injury mechanism. Two falls and one assault accounted for the remaining participants. Control group patients were admitted to the study an average of 2.7 PIDs earlier than the intervention group participants. All members of the intervention group were discharged from the medical centers to a rehabilitation facility. Two of the control group members were discharged to a rehabilitation facility, and one was discharged to a nursing home.
The pre-post GCS change score demonstrated marked improvement between groups; however, these scores were not statistically significant (intervention group = 3.3; control group = 1.0; p = .14). The mean daily GCS scores analyzed over time were also not statistically different between groups, but an interesting trajectory pattern emerged between groups. The mean daily GCS scores for the intervention was lower (6.1) and rose (6.8) over time compared to the mean daily GCS score of the control group, which began higher (7.4) and decreased over time (6.0). Difference between groups on SSAM scores, before and after the second clinical measure for arousal, was statistically significant (t = -3.03; p = .015; Table 4).
The RLA change in score for the intervention group before and after stimulation was 1.2, but no change in score was found in the control group (Table 4). The DRS score, a measure of functional ability, improved from baseline to discharge in the intervention group (18.8 to 15.1), compared to the control group (19.3 to 19.0) as reflected by the decreasing scores. The DRS change score stimulation indicated a statistical difference between groups (p = .0005; Table 4).
Combined eye and motor (EM) responses of participants receiving the sensory stimulation program were evaluated to determine whether an interaction effect occurred over time by PID, stimulation type (family voices, music, and orientation) or PID by stimulation type. Because the sensory stimulation program was started after 24 hours of stable ICP, the number of days between the injury and admission to the study was different for each participant. Thus, analysis of the effect of stimulation on EM responses was performed for each participant.
Several participants demonstrated significant responses (Table 5). Four participants (44%) had EM changes that were significant across PIDs. One participant with significant EM changes by PID also demonstrated a stimulation preference and had a significant PID by stimulation type effect. Analysis of variance revealed a significant difference in response to family stimuli (p = .043) and music (p = .023). Although this finding was not significant when the three types of stimuli were combined and compared to EM change scores, two participants demonstrated a significant response to a specific type of stimuli. One patient responded to music (p = .04), and another responded to family stimuli (p; .03).
To ensure safety and to prevent untoward effects in this critically ill sample, the study protocol included monitoring of ICP, HR, RR, and MAP before and after each intervention (Table 6). Of the nine participants enrolled in the intervention group, only four participants (44%) continued to have ICP monitors in place at the time of the intervention. In this group of participants, ICP changes were recorded after stimulation (range of change 1-5 mm Hg), but the increases were not statistically or clinically significant in any of the cases. Increases in ICP were not related to PID or stimulation type.
Data for HR, RR, and MAP were collected on all nine participants and were examined across injury days, before and after stimulation, and by stimulation type (Table 6). Five participants (55%) had significant changes across time for HR, and two (22%) had statistically significant changes by stimulation type. Six participants (66%) had significant changes across time for RR, and one patient (11%) had a significant difference in RR by stimulation type. Three participants (33%) had a significant change in MAP across time. These responses were isolated changes in cardiopulmonary status, but they were not accompanied by change in medical status nor did they require termination or postponement of the stimulation program; thus they were deemed to be of little clinical significance.
The aim of this study was to measure increases in arousal in comatose patients using an auditory sensory stimulation program, which controlled for intact auditory pathways using BAERs. In this study, an auditory SSP was safely administered to a critically ill group of participants, and a positive trajectory of improvement was demonstrated in those participants who received SSP.
The mean time for entry into the study was 9.4 days after injury for the intervention group and 6.0 days for the control group. The intervention group was admitted to the study 3.4 days later than the control group. The delay in eligibility for enrollment in the study was related to continued elevations of ICE There is no way to determine from these data whether the delay in entry to SSP was a benefit (provided brain recovery time) or a detriment (prolonged brain injury time), because both recovery and injury were occurring simultaneously (McIntosh et al., 1998).
The lack of unequivocal support for the use of sensory stimulation programs following TBI is related to the small sample. The small sample size does not provide the power necessary to suggest an interaction effect that was greater than normal recovery from a brain injury. It can only be inferred that those who received the SSP had an upward trend in arousal.
Although this study lacks the sample size necessary for robust statistical analysis, the improvement in arousal following a unimodal (auditory) sensory stimulation program early after injury was consistent with findings reported in other studies (Kater, 1989; Mackay et al., 1992; Mitchell et al., 1990; Radar et al., 1989; Wilson et al., 1991). Mitchell et al. reported similar findings in patients who received a multimodal coma arousal procedure early after sustaining brain injury (M = 7.08 days). In contrast, Kater and Radar et al. reported improvement in arousal using a multimodal sensory stimulation several weeks after injury when patients had been admitted to an acute rehabilitation program or to a nursing home.
The lack of significant findings in this report is also related to reliance on clinical measures of arousal. Although the clinical outcome measures used in this study and other similar studies are reliable and valid for clinical use, they do not provide the sensitivity necessary to measure subtle physiological changes in arousal. For example, participants were admitted to this study between RLA levels I and III and were discharged from the study at levels greater than Level III. Because RLA level provides a description of general behaviors but does not provide specific qualitative or quantitative endpoints, participants admitted to this study at Level III and discharged at Level III demonstrated no change in RLA level. Actually, small but critical changes in arousal, such as increased arousal frequency or duration, muscle tightening, and eye twitches, were occurring based on observations and SSAM scores, but these subtle changes were not captured by broad clinical outcome measures such as RLA level or GCS score. Another flaw in the use of clinical measures such as GCS, DRS, and SSAM is that they all measure the same three variables: eye opening, vocalization, and motor response, yet the instruments differ in purpose, scoring, and inclusion of other elements.
Measures that are sensitive to the physiological, behavioral, and cognitive responses of comatose patients must be identified and utilized before the effectiveness of SSPs can be judged. Such an approach also may begin to address the classic problem of differentiating brain recovery from intervention effect. Such a criticism is not reserved for an SSP alone but can be applied to any clinical research related to brain injury recovery whether in randomized clinical trials using neuroprotective agents or rehabilitation techniques (NIH, 1999). Without a sensitive, graded tool that measures change from baseline to discharge, patients are categorized as failing to progress along a continuum from coma to wakefulness. Such an outcome has significant effects not only on research findings but also on rehabilitation decisions made on behalf of brain-injured patients.
Unlike results reported by Wilson et al. (1991), most patients did not show a preference for one type of auditory stimuli over another. Two patients responded to family voices and one patient responded to music, but these effects were not sustained and the reasons for this response were not clear. Perhaps the type or duration of the stimuli was not sufficient. Or it may be that the clinical measures used to determine outcomes did not have the sensitivity and accuracy to pick up the patients' behavioral responses. Sisson (1990) reported that behavioral changes such as eye opening and extremity movement, as well as EEG changes, were inconsistent among patients exposed to auditory stimulation. Sisson attributed the inconsistencies to patient variability rather than measure insensitivity.
Sensory stimulation is an intervention, yet the dose, duration, type, frequency, and timing of the intervention have not been systematically addressed in the sensory stimulation literature. Most recommendations for devising a sensory intervention are based on integrated reviews of literature (Davis & White, 1995; Helwick, 1994), but the overall contributions of each component within the program have not been well tested. Radar et al. (1989) reported patients responded best when they were placed in an upright position and exposed to high personal contact. In this study, a unimodal stimulation method produced behavioral responses, but responses to specific types of stimuli were highly individualized. Duration of stimulation necessary to evoke behavioral responses and optimal duration between sessions were not addressed in the study but warrant further investigation.
The effects of voices and other auditory stimuli have been examined with respect to changes in cerebrodynamic and cardiopulmonary status. An issue related to safety is the cerebral hemodynamic and cardiopulmonary responses during sensory stimulation. In this study, auditory stimulation was not found to affect ICP, HR, RR, or MAP. These results are similar to those reported by Johnson et al. (1989), Prins (1989), Schinner et al. (1995), and Trealor et al. (1991), indicating that auditory stimuli was not a significant factor in ICP and CPP changes. Although no participants suffered adverse effects from stimulation in this study, changes in medical conditions such as sepsis, paralytic ileus, bowel obstruction, and respiratory changes occurred, and treatments for these conditions superseded the research protocol. It is important to be aware that undiagnosed medical problems or complications could decrease responsiveness and thereby blunt the effect of the sensory stimulation program. Likewise, changes in cerebrodynamic or cardiopulmonary status could be occurring independently of the sensory stimulation intervention, but changes in ICP or BP could inadvertently be described as an untoward effect from the stimulation program rather than a change in medical condition (improving or deteriorating).
Limitations and Directions for Future Research
There are several serious limitations embedded in this study The first is the sample size. There is not sufficient power to make between- or within-group comparisons. The second limitation is the lack of sensitive measures for detecting subtle changes in arousal. The third limitation is the inherent dilemma associated with the natural course of brain injury recovery versus the plastic recovery associated with increased stimulation.
Continued efforts to address the effects of SSP early after brain injury are needed. Suggested areas for continued sensory stimulation research in critically ill patients include testing a variety of unimodal and multimodal programs for dose and duration effects, developing outcome measures that are sensitive to subtle behavioral changes in arousal, and performing long-term follow-up to compare cognitive and behavioral outcomes across time.
The recent National Institutes of Health consensus conference on "Rehabilitation of Persons with Traumatic Brain Injury" endorsed the need for continued efforts to improve care at all levels of recovery in order to restore functional outcome (NIH, 1999). Most of the clinical research is fraught with complications, and an inability to distinguish brain recovery from intervention effect is not a problem unique to sensory stimulation research. Despite sample size and confounding variables, participants in this study exposed to an early SSP demonstrated a positive recovery of function trajectory without compromising cerebral dynamic and cardiopulmonary function.
This research was supported by the National Institute for Nursing Research #5R15NR0377302 and by the Bryan W. Robinson Foundation. Special thanks to Soohyun Park for her assistance in preparing the manuscript.
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Questions or comments about this article may be directed to: Alice E. Davis, PhD RN, by phone at 734/763-5650 or by e-mail at email@example.com. She is an assistant professor at the University of Michigan School of Nursing, Ann Arbor, MI.
Ana Gimenez, MS RN, is a professor at Puerta de Hierro, Clinica Puerta de Hierro, Madrid, Spain.
Table 1. Type and Duration of Auditory Stimuli Duration, Type minutes Orientation and commands 5 Bells, blocks, and claps 5 Music (favorite or researcher selected) 15 Familiar voices (taped) 10 Television or radio 10 Table 2. Demographic Data and Type of Brain Injury by Participant Entry Group Age PID GCS Score Injury Type Intervention 19 5 4 CHI, shear injury, intracerebral hemorrhage 35 10 8 SDH (fronto-parietal) 45 9 3 EDH, SDH, contusions 37 5 8 SDH, SAH, bi-frontal contusions 30 8 7 CHI, shear injury 25 7 7 SDH, contusions, skull fracture 40 8 7 Temporal contusions (bilateral) 17 18 7 Intracerebral hemorrhage 17 13 4 CHI, shear injury, temporal contusions Mean 30 9 5.5 Control 49 8 5 SDH, temporal contusions 23 5 6 SDH, contusions 19 5 7 EDH, depressed skull fracture Mean 30 6.3 6 Other Injury Injuries Mechanism Intervention No MVC No MVC No Fall No Assault Yes MVC Yes MVC Yes Fall No MVC Yes MVC Mean Control No MVC Yes MVC Yes MVC Mean Key PID = Postinjury day CHI = Closed head injury GCS = Glasgow Coma Scale SDH = Subdural hematoma EDH = Epidural hematoma SAH = Subarachnoid hemorrhage MVC = Motor vehicle collision Table 3. Mean Age, ISS, PID, and GCS Score of the Intervention and Control Groups Intervention Control Group Group (n=9) (n=3) Mean age 30 30 Mean ISS 19.5 20 PID 9 6.3 Mean GCS Score 5.5 6 Table 4. Mean Change in Scores for GCS, RLA, DRS, and SAM and Range for Mean Daily GCS Scores for the Intervention and Control Groups Intervention Control Group (n=) Group (n=3) p Glasgow Coma Scale 3.3 1.0 .278 Ranchos Los Amigos Level of 1.2 0 Cognitive Functioning Scale Disability Rating Scale 3.7 0.3 .0005 Sensory Stimulation Assessment Measure 11 0.3 .015 Table 5. Eye-Motor Scores by Patient for Postinjury Day (PID), Stimulation Type, and PID by Stimulation Type Stimulation PID x Stimulation PID Type Type f value p value f value p value f value p value 52.51 .0001 3.21 .050 4.15 .022 22.91 .0001 0.07 .93 0.08 .92 7.70 .009 0.71 .49 0.97 .38 7.08 .020 1.59 .24 1.58 .24 3.85 .056 0.07 .93 0.15 .86 0.51 .48 0.58 .56 0.72 .49 1.37 .24 0.75 .47 0.72 .49 2.38 .12 2.71 .07 2.47 .09 12.17 .001 2.19 .12 2.68 .081 PID Significance of f value p value Stimulation Type 52.51 .0001 Family: f =-2.08, p =.043 Music: f=-2.35, p =.023 22.91 .0001 7.70 .009 7.08 .020 3.85 .056 0.51 .48 1.37 .24 2.38 .12 Family: f= -2.20, p = .03 12.17 .001 Music: f= .08, p= .04 PID x Stimulation Type = PID x Stimulation Type Table 6. fand p Values for Heart Rate, Respiratory Rate, Mean Arterial Pressure and Intracranial Pressure by Post Injury Day, Change Score (Pre/Post Intervention), and Stimulation Type Heart Rate Pre/ Stimulation PID post Type f p f p f p 74.7 .000 0.03 .86 0.96 .38 7.22 .009 0.20 .65 1.59 .21 78.3 .000 0.03 .86 3.72 .29 0.05 .81 0.01 .93 0.54 .58 1.60 .20 0.14 .70 0.32 .72 22.6 .000 0.56 .45 2.96 .056 0.24 .62 0.01 .93 1.68 .19 0.10 .74 1.15 .28 0.53 .58 7.50 .007 0.24 .62 1.52 .22 Respiratory Rate Pre/ Stimulation PID post type f p f p f p 5.22 .24 0.10 .74 0.87 .42 42.9 .000 0.17 .68 0.64 .52 41.3 .000 0.000 .96 0.24 .78 2.28 .14 0.02 .87 1.92 .16 0.44 .55 0.25 .61 3.70 .028 2.93 .09 0.03 .85 0.34 .71 60.3 .000 0.00 .97 0.47 .62 22.8 .000 1.39 .23 1.06 .347 7.88 .006 0.24 .62 0.64 .52 Mean Arterial Pressure Pre/ Stimulation PID post type f p f p f p 0.67 .46 0.11 .74 2.26 .11 0.23 .63 0.03 .86 2.37 .10 1.00 .32 0.17 .67 0.25 .78 24.5 .000 0.01 .99 1.45 .25 0.03 .86 0.02 .89 1.68 .19 122 .000 0.02 .90 0.20 .81 2.96 .08 0.79 .37 0.53 .59 20.4 .000 0.07 .79 1.18 .31 1.58 .21 0.06 .81 1.50 .23 Intracranial Pressure Pre/ Stimulation PID post Type f p f p f p 0.02 0.90 0.07 .80 0.42 .67 -- -- -- -- -- -- 0.02 .67 0.07 .35 0.42 .32 2.31 .14 0.43 .51 1.65 .21 -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- -- 0.83 .36 0.58 .44 2.50 .086 -- -- -- -- -- -- Key PID = postinjury day Pre/post = change score/before and after stimulation Stimulation/type = change score/before and after stimulation .000 = .0001
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