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Caloric stimulation in neglect: Evaluation of response as a function of neglect type

Published online by Cambridge University Press:  12 February 2004

JOHN C. ADAIR ,
DUK L. NA ,
RONALD L. SCHWARTZ  and
KENNETH M. HEILMAN
JOHN C. ADAIR
Affiliation:
Department of Neurology, University of New Mexico and Albuquerque VA Medical Center, Albuquerque, New Mexico
DUK L. NA
Affiliation:
Department of Neurology, Sung Kyun Kwan University College of Medicine and Samsung Medical Center, Seoul, Korea
RONALD L. SCHWARTZ
Affiliation:
Department of Neurology, 3 Hattiesburg Clinic, Hattiesburg, Mississippi
KENNETH M. HEILMAN
Affiliation:
Department of Neurology, 3 Hattiesburg Clinic, Hattiesburg, Mississippi
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Abstract

Contralesional neglect may be induced by either unawareness of contralesional stimuli (attentional neglect, AN) or failure to act in contralesional space (intentional neglect, IN). We examined whether contralesional cold caloric stimulation differentially affects AN versus IN. Patients with left-sided neglect (n = 16) from right-hemisphere lesions performed target cancellation and line bisection tasks. Using a video-based apparatus that reverses the right and left side of stimuli, patients with abnormal cancellation performance were divided into those with AN and those with IN. The 5 subjects with normal cancellation performance but rightward bisection bias were also separated into 2 neglect groups. Subjects performed cancellation or bisection tasks before and immediately after irrigation of the left auditory canal with ice water. Caloric stimulation induced brisk rightward nystagmus in all subjects. Subjects with AN cancelled more left-sided targets after stimulation than those with IN (p = .02). Whereas caloric stimulation significantly shifted bisection error leftward for both IN and AN groups (p < .0001), AN patients exhibited a greater magnitude of shift than the IN patients. While the basis for differential performance remains undefined, the data indicate that caloric stimulation influences AN more than IN. (JINS, 2003, 9, 983–988.)

Keywords

Caloric stimulationNeglect
Type
Research Article
Information
Journal of the International Neuropsychological Society , Volume 9 , Issue 7 , November 2003 , pp. 983 - 988
Copyright
© 2003 The International Neuropsychological Society

INTRODUCTION

The neglect syndrome results when brain injury disturbs an individual's capacity for interaction with the environment that does not relate to defects in elementary sensory and motor function (Heilman et al., 1993). Most elements of neglect display specific spatial characteristics, with misapprehension of stimuli mainly from the space opposite an injured cerebral hemisphere. In their usual surroundings, neglect can prevent patients from finding food on half their plate, dressing and grooming half of their body, and negotiating obstacles in their path. In the clinic, neglect can be detected through tasks in which patients fail to locate half the items in an array, copy only half of a simple figure, and misbisect line stimuli, suggesting that they lack awareness of or fail to act on a portion of the stimuli (Albert, 1973; Schenkenberg et al., 1980).

Despite years of extensive observation and study, the neuropsychological basis for neglect phenomenon remains imprecisely defined. One elementary account separates patient performance in both home environment and in clinical tests into two primary forms. At one end of the spectrum, attentional neglect (AN) refers to failure of processes responsible for perception of contralesional stimuli. In contrast, intentional neglect (IN) implies a failure of processes responsible for directing responses in or toward contralesional space (Milner & Harvey, 1994). Attentional and intentional forces presumably work in concert under usual circumstances. Several methods of pitting these processes against each other indicate different types of dysfunction can be operative in different neglect patients and, more importantly, that different forms of neglect result from injury to anatomically distinct regions. In brief, AN tends to follow injury in parietal regions while IN correlates with lesions in frontal and subcortical structures (Bisiach et al., 1990; Coslett et al., 1990; Tegner & Levander, 1991).

Thus, despite a common clinical appearance, malfunction in different neural systems may in fact create nosologically different forms of hemispatial neglect. Aside from broad anatomic distinctions, few other facts support such a biological basis for subclassification of neglect. A relevant issue pertaining to the validity of separating neglect into distinct subtypes relates to whether a given therapeutic intervention influences different subtypes of neglect to the same extent.

Evidence suggests that various interventions, such as cold caloric stimulation (CCS) of the contralesional ear (Cappa et al., 1987; Rubens, 1985), temporarily ameliorate neglect behavior. The physiologic mechanism by which such treatments exert their effect remains unknown. Since CCS temporarily shifts the position and movement of the eyes, head, and trunk, it may simply extend the range of movements into the neglected space. This account might predict a disproportionate influence on patients with IN. Alternatively, CCS might rectify spatially constrained deficiencies, such as the hypothetical distortion of the representation of contralesional space (Bisiach & Luzzatti, 1978). This account might result in disproportionate influence on patients with AN and limit its effect to interactions with space opposite the injured hemisphere. If CCS affects non-lateralized arousal systems (Robertson, 1993), then there may be no differential effect, either in terms of neglect subtype or regarding improvement in the ipsilesional versus contralesional space.

The present study examines whether CCS differentially impacts neglect subtypes, as defined through the AN versus IN dichotomy.

PATIENTS AND METHODS

Subjects included 16 unselected patients with left-sided neglect following cerebrovascular injury to the right hemisphere. All patients were right-handed by self-report. The group consisted of 9 men and 7 women with a mean age of 64.5 years (Table 1). Patients were recruited from Shands Hospital at the University of Florida or the Samsung Medical Center at Seoul National University. The sample was taken from a larger group screened at each medical center. All procedures described below were conducted during the acute hospitalization or within 30 days of injury onset. Neglect was considered present if patients demonstrated either any contralateral omissions on the Albert line cancellation task (Albert, 1973) or rightward line bisection beyond the 95% confidence interval for normal subjects. After obtaining informed consent, patients underwent additional testing to determine neglect subtype.

Clinical details

The technique used to distinguish between attentional and intentional neglect has been described in detail elsewhere (Na et al., 1998). In brief, the apparatus consists of a closed circuit video camera mounted above and below a clear Plexiglas surface. Subjects performed line bisection and cancellation tasks while viewing stimuli on a 30.5 cm monitor at a distance of 500 mm. A stimulus page on the monitor therefore subtended approximately 35 degrees of visual angle in central vision. Lines for bisection were 230 mm long and 3 mm thick. The cancellation array consisted of 40 black lines (25 mm length, 0.5 mm thick) of various orientations that were dispersed in a random array, including 18 lines on each half of the page and 4 central lines that were not included in data analysis. The direct condition (DC) used an image projected from the overhead camera. In the DC, the left side of the stimulus object was on the left of the screen and the right side of the object was on the right of the screen. Movements on the surface were thereby spatially congruent with those displayed on the monitor. Projecting from the other camera resulted in the indirect condition (IC). In the IC, the left side of the paper projected to the right side of the monitor and vice versa. Consequently, leftward movements on the surface appear as rightward movements on the monitor and vice versa. Separation into AN or IN was based upon whether or not bias shifted between the DC and IC. For example, persistent rightward bisection bias or omission of targets from the left side of the array in the IC suggests a failure to move in or toward left space (IN). Alternatively, if the IC shifts bisection to the left of midline or produces omission of targets from the right side of the array, then the patient demonstrates defective perceptual processing of the left side of the monitor (AN).

Patients with abnormal performance on line bisection and target cancellation were given a series of identical tasks with the video device. Some patients located all targets on the cancellation task but showed rightward bisection error; these patients were administered additional line bisections through the video apparatus. As depicted in Table 2, all patients demonstrated rightward line bisection of varying magnitudes. Bisection error fell outside the 95% confidence interval for normal performance in every case. Abnormal performance on target cancellation occurred in 11/16 patients. Again, the number of omissions in left space varied, but normal subjects find every target in the Albert line cancellation task (Albert, 1973).

Effect of caloric stimulation on mean line bisection error

On another day, usually one day later (range 1–7 days), the patients were brought back to the laboratory. Examiners performed otoscopic inspection of the left external auditory canal and bedside assessment of auditory acuity differences between the two ears. Next, patients were given CCS according to standard clinical methods. Specifically, patients were tilted backward in their wheelchair to an angle of approximately 45° from vertical. A volume of ice water (30 ml) was slowly infused into the left external canal via silastic catheter advanced into proximity of the tympanic membrane. The infusion rate was approximately one ml/s. Immediately after irrigation was complete, the patient resumed a sitting position in front of the video apparatus. Examiners rapidly assessed gaze in midposition for the development of nystagmus. If the first irrigation failed to evoke nystagmus, the catheter was repositioned and the infusion was repeated.

Once nystagmus was verified, patients were asked to perform either line bisection or target cancellation using the video apparatus. Patients performed 10 bisection trials before and after caloric stimulation; the number of cancellation patterns varied between 1 and 2 depending on how rapidly patients completed the task. Each cancellation trial was limited to 5 min, after which time the maximal stimulation effect had likely dissipated. Only 3 of 11 subjects with both abnormal cancellation and bisection consented to perform both tasks after CCS. For this group, another infusion of cold water was administered between tasks to renew the stimulation effect. In total, the caloric stimulation effect on line bisection was assessed in 13 patients and target cancellation in 6 patients.

Data was analyzed using a mixed model analysis of variance (ANOVA). For line bisection, bisection error was measured to the nearest .5 mm. Following convention, rightward errors were given positive values and leftward errors were given negative values. The effect of CCS on line bisection was tested using univariate ANOVA. Bisection error was the dependent variable while neglect type was the grouping variable. For target cancellation, the dependent variable was the difference between the number of targets cancelled in the stimulated condition minus the baseline performance. A two-level analysis was performed using stimulus page space (right side vs. left side) as the within-subjects factor and neglect type (AN vs. IN) as the between-subjects factor. Significant main effects were explored with post-hoc testing using the Tukey test when appropriate.

RESULTS

Comparison of lesion location (Table 1) with neglect type (Tables 2 and 3) provided information regarding approximate clinico-anatomic correlates. Designating lesions confined to the frontal lobe or basal ganglia as anterior and lesions involving the thalamus or the temporal, parietal, or occipital lobes as posterior, all but Patients 13 and 16 could be unambiguously classified. In the remaining 14 patients, the predominant lesion site was anterior in seven and posterior in seven. In the 10 patients with AN on line bisection, 7 demonstrated posterior brain injury; 2 others harbored anterior lesions, and the final patient's infarct involved the entire middle cerebral artery territory. Conversely, of 3 patients with IN during the bisection task, 2 showed anterior injuries while the other involved both anterior and posterior structures. Despite smaller numbers, similar results were obtained examining neglect type based on cancellation performance. Scans from 2 of 3 patients with AN on the cancellation task revealed posterior lesions. Lesions from all 3 patients with IN involved anterior structures, though 1 patient's lesion also involved the parietal lobe.

Effect of caloric stimulation on target cancellation

Table 2 displays the effect of CCS on mean line bisection error for both neglect groups. Stimulation ameliorated neglect in 12 of 13 patients. Considering the entire sample, the main effect of CCS was significant by univariate ANOVA [F(1,258) = 98.8, p < .001]. In the AN group (n = 10), stimulation shifted line bisection error toward the left side in every case. In 5 of 10 cases, the stimulated judgment was actually to the left of true midpoint and the mean stimulated judgment for the group was 3.6 mm left of center. The amount of baseline deviation did not appear to influence the magnitude of the leftward shift (r2 = .38, p = .28).

The 3 patients with IN differed greatly in their response to CCS. One patient shifted bisection error to the left of true midpoint, another patient shifted leftward while remaining right of true midpoint, while the final subject demonstrated increased rightward displacement of mean bisection error.

The interaction between stimulation state (baseline vs. stimulated) and neglect type (AN vs. IN) was significant [F(1,256) = 20.7, p < .001], suggesting between-group differences in response to the intervention. Post-hoc analysis demonstrated that stimulation significantly influenced bisection performance for the AN group (p < .001), while the pre- and post-stimulation performances were not significantly different for the IN group (p = .77). Because the 3 patients in the IN group responded in completely different fashion from each other, the analysis was repeated using only data from the 2 subjects with reduction in bisection error. This resulted in an even greater main effect of stimulation [F(1,238) = 128.7, p < .001]. The Treatment × Neglect Type interaction remained significant [F(1,236) = 5.4, p = .02]. Post-hoc contrasts now demonstrated a marginally significant (p = .04) effect of stimulation for the IN group.

The influence of CCS on target cancellation is depicted in Table 3. The 6 patients comprised 3 patients in each neglect group. In the contralesional (i.e., left) hemispace, both groups omitted many or all of the targets prior to stimulation; there was no significant between-group difference in baseline omissions. In contrast, at baseline before stimulation, patients with AN cancelled more targets from the ipsilesional half of the array than did patients with IN (M 16.0 vs. 7.3). Hence, in contralesional space, the severity of neglect was comparable in both groups but, for unclear reasons, ipsilesional target cancellation appeared more disrupted in the IN group.

In patients with AN, CCS resulted in substantial improvement in target cancellation from the contralesional half of the array. One patient actually achieved a normal level of performance after stimulation. The IN group showed no change in performance with stimulation for targets in the contralesional space. The ANOVA demonstrated a significant interaction between Stimulus Page Space × Neglect Type [F(1,8) = 11.6, p = .009). Post-hoc analysis demonstrated that CCS produced a significantly (p = .019) greater response for patients with AN compared to those with IN only for targets located in the contralesional half of the array.

In the ipsilesional half of the array, stimulation actually resulted in modest improvement in the number of targets canceled in the IN group (M 7.3 before vs. 10.3 after). Since AN patients performed essentially at ceiling levels prior to stimulation, we could not reliably conduct between-groups comparisons of the effect of CCS on cancellation of targets from the ipsilesional space.

DISCUSSION

Rubens (1985) felt that CCS attenuated neglect behavior through induction of a transient “leftward motor bias.” In support, he noted that the effect of this intervention seemed proportional to the amount of facilitation of left lateral gaze. The only patient who failed to improve following stimulation was also the patient who failed to show nystagmus, presumably because of vestibulopathy. Similarly, patients showing partial reversal of neglect dyslexia and the most modest improvements in a target cancellation task were also those who had “minimal” restoration of leftward eye movements. Rubens concluded that CCS acted through opposition of the impact of hemispatial hypokinesia on tests of neglect behavior.

Subsequent research suggests that Rubens' original interpretation may have been too narrow. For example, the work of Vallar and colleagues (1990) demonstrates how cold CCS can favorably alter somatosensory thresholds on a tactile detection task and reduce tactile extinction. In another study, the same researchers showed that CCS attenuates neglect, even on paradigms such as tactile exploration without visual guidance (Vallar et al., 1993). Cappa et al. (1987) reported that CCS temporarily ameliorates both hemiasomatognosia for the weak limb and increases awareness of deficit in patients with dense anosognosia. At least two separate groups have also documented how CCS temporarily attenuates somatoparaphrenic delusions (Bisiach et al., 1991; Rode et al., 1992). In all of these examples, the effect of CCS on behavior does not necessarily require either visual input or motor-exploratory output. Hence, the data persuasively indicate that the impact of CCS on neglect extends far beyond the influence of shifting gaze toward the contralesional hemifield or opposition of hemispatial hypokinesia.

When Rubens published his results, he had no means for directly testing the hypothesis that CCS opposed premotor factors that contribute to neglect behavior. Subsequent methods were developed which, by pitting the location of movement and action against the location of visual perception, provided a crude distinction between so-called intentional neglect (IN) and attentional neglect (AN; Bisiach et al., 1990; Coslett et al., 1990; Tegner & Levander, 1991). Radiographic correlations supported the notion that IN was most commonly associated with injuries to motor association cortex, its subcortical projections, or the target of these projections such as the basal ganglia (Ladavas, 1994). In contrast, the cerebral infarcts in Rubens study all involved portions of the parietal cortex and adjacent posterior association cortex, brain regions most commonly associated with AN. Hence, data from Rubens' original study could be interpreted, albeit through retrospective inference, as supporting the notion that CCS opposed sensory-perceptual factors contributing to the attentional type of neglect.

Using a video-based technique, we directly tested for differential effects of CCS on attentional and intentional neglect. Given the small sample size, the results must be considered preliminary and interpreted conservatively. Nevertheless, we observed intergroup differences on both line bisection and target cancellation tasks. For line bisection, CCS shifted bisection marks to the left for both groups. The mean change produced by stimulation was greater for the AN group than the IN group. However, the latter set included one patient whose performance actually shifted more to the right after stimulation, a result never observed in AN patients. After excluding this individual, intergroup differences were much less pronounced, though the same trend persisted. Differential responsiveness was much more apparent with target cancellation tasks. The AN group greatly improved their performance after CCS while the IN group showed only modest change. Since the latter patients omitted more targets at baseline, the present data cannot exclude the possibility that severity of neglect might actually be the critical determinant of CCS response. However, mean line bisection error was actually greater at baseline for the AN group, providing indirect evidence against this conjecture. Interestingly, IN patients increased target cancellation much more for the ipsilesional side compared to the contralateral side, a phenomenon for which we have no explanation. In aggregate, the data indicate that CCS may modify performance on clinical tests of neglect more for patients with AN than for IN.

While the dichotomy we have drawn between AN and IN is highly simplistic, our results might help integrate the perceptual/premotor framework into other accounts of neglect behavior. For example, if neglect simply resulted from “motor bias” to the right (or away from the left), and had no influence on non-lateralized arousal systems, then CCS should increase cancellation of leftward targets while reducing cancellation of rightward targets. Furthermore, one might predict greater gains for the IN group. Neither situation was observed in the current study. If CCS simply reduces neglect from augmentation of non-specific arousal systems, then CCS should improve target cancellation in both ipsilesional and contralesional space, with a proportionately greater impact on ipsilesional space. According to our data, this may pertain more to patients with IN than AN. Last, if neglect results primarily from disruption of a mental representation of contralesional space and CCS acts to bolster or restore this representation, then target cancellation performance should improve primarily in contralesional space. According to present observations, such an account may pertain primarily to the AN group.

The biological basis for the effect of vestibular input on spatial perceptual processing remains obscure. The relevant anatomy begins with vestibular afferents, synapsing in the thalamus and projecting to a limited number of discrete cortical areas. From radionuclide studies, irrigation of the external auditory canal with warm water reliably leads to increased cerebral blood flow in a discrete portion of the contralateral posterior superior temporal lobe (Friberg et al., 1985). Cortical stimulation studies by Penfield and Jasper (1954) suggested that the pertinent region actually occupies the depths of the Sylvian fissure, medial to the temporal planum. Recently, Brandt and colleagues (1994) found a strong association between abnormal vestibular sensation and injury to the posterior insular cortex and the adjacent superior temporal or transverse temporal gyri. The areas of cerebral cortex receiving vestibular projections therefore appear to be located anatomically adjacent to the inferior-posterior parietal cortex, the most common anatomic correlate of the neglect syndrome. However, anatomic attributes of vestibular cortex may not be as relevant as its functional characteristics, including its interaction with other sensory modalities.

Stimulation of the vestibular system in natural contexts always involves concomitant modulation of activity in multiple convergent sensory channels. Whereas other sensory modalities undertake preliminary analysis of physical properties in relative isolation, the nature of vestibular stimuli (i.e., angular acceleration of the head) guarantees that they are ordinarily yoked to associated visual and somatosensory stimuli. In other words, the vestibular apparatus provides body displacement data that essentially duplicates or copies that induced in somatosensory and visual systems. Microelectrode recordings from vestibular cortex furnish a neuroanatomic substrate for this cross-modal interface, showing that the neurons respond not only to vestibular stimuli, but also to visual and tactile afference (Grusser et al., 1990). Recent PET studies also demonstrate increased blood flow to the perisylvian and supplementary somatosensory areas, basal ganglia, and cingulate cortex contralateral to CCS (Bottini et al., 2001). By means that are not yet clear, input provided through vestibular channels may somehow supplement or supplant other damaged sensory inputs that usually contribute to multimodal egocentric spatial representations (Karnath, 1994). Functional imaging data are also compatible with the interpretation that CCS may ameliorate neglect through activation of other components of the distributed network (e.g., cingulate, basal ganglia) that subserve motor-exploratory aspects of spatial cognition (Heilman et al., 1993; Mesulam, 1998).

Alternatively, the influence of CCS on spatial cognition may also result through depression of activity in other sensory systems. Functional imaging studies provide evidence of a reciprocal interaction between visual and vestibular processing; CCS reduces cerebral blood flow in bilateral striate and extrastriate visual cortex (Bottini et al., 2001). Maximal deactivation occurs in visual association cortex (V2/V3) ipsilateral to stimulation, an observation corroborated physiologically through ipsilateral suppression of alpha power after CCS (Storrie-Baker et al., 1997). Reciprocal suppression may normally serve some role in perceptual functions such as the discrimination between self versus environmental motion (Brandt et al., 1998). After brain damage responsible for neglect, however, relative reduction of early visual operations in the healthy hemisphere may actually facilitate residual contralesional spatial processes in the damaged hemisphere. Such a mechanism could explain why some patients with neglect actually shift their bisection bias beyond midpoint into the “normal” space, a phenomenon not predicted through simple restitution of a distorted representation of space.

Finally, from a clinical perspective, differential responsiveness to specific interventions forms an elementary basis for the development of a more systematized nosology of the neglect syndrome. Failure to account for different neglect types may explain why rehabilitation studies often report equivocal results for a single treatment on a large, presumably heterogeneous group of patients with the neglect syndrome (Robertson et al., 1993). Ideally, greater specificity in the determination of neglect subtypes might lead to more rational grounds for application of tailored interventions and therapies. For example, on the basis that parietal lesions produce deficits primarily in covert or involuntary orientation, Ladavas and colleagues (1994) recently described a successful treatment program that emphasized volitionally directed mechanisms of orientation. To what degree such strategies impact neglect subtypes as defined herein remains an important empirical question.

ACKNOWLEDGMENTS

This work was supported by Samsung Grant #SBRI C-96015 (DLN) and by the Medical Research Service of the Department of Veterans Affairs (KMH).

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Figure 0

Clinical details

Figure 1

Effect of caloric stimulation on mean line bisection error

Figure 2

Effect of caloric stimulation on target cancellation