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Show Journal of Newo- Ophthalmology 18( 4): 263- 267, 1998. & 1998 Lippincoll Williams & Wilkins, I'hiladolphia Visually Induced Reactivity in Posterior Cerebral Artery Blood Flow Babette Spelsberg, M. D., Andrea Bohning, M. D., Detlef Kompf, M. D., and Christof Kessler, M. D. To evaluate visually induced reactivity ( VIR) in the posterior cerebral artery ( PCA), mean flow velocities in the PCA were measured bilaterally in 35 normal subjects and in 17 patients with PCA territory infarctions, by means of transcranial Dopp-ler ultrasound. After the individual PCA baseline flow was estimated, different visual stimuli were applied: on- off light, colored light, complex scene, and visual imagery task, and the C02 test was administered. A sampling rate of 20 Hz was used, and the raw data were transferred to a computer. The baseline flow and the maximum flow increase were calculated with a specially designed program. In control subjects, the on- off light stimulus induced a mean increase in PCA flow velocities of 21.5 ± 6.4%, and colored light induced an increase of 22.3 ± 6.3%. Complex scenes significantly elevated VIR more than light and colored light, with a mean increase of 28.8 ± 6.8% ( p < 0.05). Mental imagery had no significant effect on PCA flow velocities. There was no significant difference in flow between the right and left PCA in healthy subjects. In patients with PCA territory infarctions with homonymous hemianopsia or qua-drantanopsia, there was a marked decrease of VIR and C02 reactivity on the affected side corresponding to the extent of PCA territory infarction. Visual stimuli increased blood flow velocity bilaterally in the PCA, which supply the visual cortex and visual association area. This noninvasive test seems to be well suited to normal subjects and to patients with vascular disorders affecting the PCA. Key Words: Brain metabolism- C02- Posterior cerebral artery territory infarction- Transcranial ultrasound- Test- Visual stimulation. Cerebral blood flow ( CBF) depends on the state of brain activation and ranges between 40 ml per 100 mg brain tissue per minute at rest to 125 to 135 ml per 100 mg brain tissue per minute at excitation ( 1). Positron emission tomography studies ( 2,3) have demonstrated that visual stimulation differentially increases local me- Manuscript received August 27, 1996; accepted May 13, 1998. From the Department of Neurology ( B. S., C. K.), University of Greif-swald, Germany; and the Department of Neurology ( A. B., D. K), Medical University of Liibeck, Germany. Address correspondence and reprint requests to Prof. Dr. C. Kessler, Department of Neurology, Ernst- Moritz- Arndt University of Greifs-wald, Ellernhob. str, 1- 2, D- 17487 Greifswald, Germany. tabolism in the visual cortex as a function of stimulus complexity. In hemianopic patients the local cerebral metabolic rate for glucose is reduced in the visual cortex ( 3). Transcranial Doppler sonography ( TCD) has also been used to investigate the dynamics of cerebral blood flow by recording flow velocities in the basal cerebral arteries. This method has the advantage of excellent temporal resolution ( 4,5). Aaslid ( 6) was the first to study the dynamics of cerebral blood flow in the posterior cerebral artery ( PCA) in response to stimulation with light. A study by Urban et al. ( 7) showed that occipital lobe infarctions of different degrees of severity limit the visually activated blood flow increase in the ipsilaleral PCA. It is well known that blood flow reactivity to visual stimulation is specific to the PCA supplying the visual cortex ( 6- 8). A small increase in blood flow in the middle cerebral artery ( MCA) caused by visual stimulation has also been noted, but this increase does not exceed 7% ( standard deviation ranges between 3% and 8%) and is likely to be based on nonspecific effects, such as attention and arousal ( 6- 8). Acute hypercapnia induces immediate acidosis of the cerebrospinal fluid and brain cells. The direct effect of C02 and acidosis is dilatation of muscle cells of the cerebral arterioles, which increases cerebral blood flow ( 9). Single photon emission computed tomographic studies and reports on patients with various brain lesions ( 10- 13) show that left inferior occipital regions play a prominent functional role in visual mental imagery. Because the left inferior occipital cortex consists mainly of the primary and secondary visual cortices, and because the PCA is the source of its blood supply, we tested whether a visual imagery task would increase blood flow velocity in the left PCA. We wanted a detailed evaluation of the visually induced reactivity ( VIR) of blood flow in the PCA in response to different visual stimuli, visual imagery tasks, and C02 stimulation in normal subjects and in patients with PCA territory infarctions. The objective of our study was to investigate whether the increase in flow velocity during activation is correlated with the complexity of the applied stimulus and whether a reduction of VIR occurs in patients with PCA infarctions. 263 264 B. SPELSBERG ET AL. SUBJECTS AND METHODS We used as controls 19 young subjects with a mean age of 24.3 ± 1.5 years. Among these were 10 men and 9 women with no sign of cerebrovascular or ophthalmologic disease. Some subjects had myopia and wore their glasses during VIR measurements. To test whether VIR is age dependent, a second group of 16 older subjects with a mean age of 54.9 ± 11.9 years was investigated. These patients were recruited from the neurology inpatient clinic. They showed no signs of cerebrovascular disease or dementia. Visual acuity was normal, assessed by reading from a chart. Patients with PCA Territory Infarctions Seventeen patients with PCA territory infarctions ( mean age, 60.2 ± 11.9 years) were included in our study. All had hypodense lesions in the occipital region, revealed by cranial computed tomographic scan. Ten patients had complete homonymous hemianopsia, and seven had quadrantanopsia. Ten PCA territory infarctions were on the right side, and seven were on the left side. Two patients with bilateral PCA territory infarction were not included in the study because the intent was to compare the nonaffected side with the affected side. In eight patients the examination was performed within 4 weeks after the stroke, and in the other nine patients the interval between stroke and examination was approximately 2 years. Experimental Setting Studies were carried out in a dark and quiet room. Subjects sat comfortably and relaxed in a chair and looked at a screen 2 m in front of them on which the different visual stimuli were presented. They were asked to keep their eyes closed between the tasks and to open them for stimulation. To minimize artifacts induced by the environmental setting, the laboratory was absolutely dark, and the projected slide stimuli occupied approximately 80% of the visual field. The remaining 20% was occupied by the surrounding dark room. There was no conversation during the measurements except for short commands to open or close the eyes. The TCD recordings were taken from the left and right PCA, successively. The conditions of the experiment were the same for all participants. A TCD device ( TC 2000S; EME GmbH, Uberlingen, Germany) was used, with a 2- MHz probe. The ultrasound intensity was 100 mW/ cm2, and the sampling rate was 20 Hz. A durable probe was installed, and the intracranial PCA was insonated through the transtemporal window. The MCA was identified at a depth of 50 mm. Then the probe was turned to a backward position, and the PCA was insonated at a depth of 62 ± 2 mm, based on the characteristic velocity spectrum and specific response to light stimulation. One young subject screened for participation could not be included because the transtemporal window on the left side could not be obtained. In all other participants the characteristic signal of the PCA was found. Flow velocities were measured continuously with subjects at rest. These constant values formed the individual baseline flow velocities. Different stimuli were then applied: • On- off light: After a rest phase with closed eyes, the slide projector was turned on with no slide for 25 seconds, and the subjects were asked to look at the lighted screen. • Colored light: Red, blue, or green was projected on the screen for 25 seconds, and the subjects were asked to look at it. • Complex scene: A landscape scene was projected on the screen for 25 seconds. • Visual imagery task: The subjects were asked to imagine a scene, preferably from their last holiday, or any other scene as vividly as possible for 40 seconds with their eyes closed. Light intensities of the different visual stimuli were assumed to be constant because the same slide projector was always used. All stimuli were applied after the flow velocities had reached baseline. In addition to the VIR measurement, vasomotor reactivity of each PCA was estimated by the C02 test. The subjects breathed a mixture of room air and 33% Oz through an anesthesia mask. The mean flow velocity in the PCA was measured for several minutes, and the baseline flow velocity ( VR) was calculated. Then, C02 was continuously added until an end- tidal C02 concentration of 8% was obtained. At this point the maximum flow velocities ( Vmax) were recorded, and the cerebral vasomotor reactivity was calculated as follows: VR% = ( Vmax - VR) x 100 H- VR. These results were compared with the percentage increase of PCA flow velocities after visual stimulation. During visual stimulation, flow velocity values were recorded continuously, and the raw data were stored for later evaluation. The data were calculated by the standard algorithm implemented on the Doppler device and exported to an ASCII file. We designed a program in Turbo Pascal ( Borland Int., Scotts Valley, CA) for further data processing. First, a running average was calculated from the data. Then the increase in blood flow velocity was analyzed. If it exceeded 12% of the baseline flow, the average of the following 70 values was interpreted as the maximum value. This threshold was established to allow measurement of the specific visual effects, because it is known that the nonspecific effects such as attention and arousal lead to an increase in blood flow velocity of up to 7%. To be on the safe side, another 5% was added, which was approximately one standard deviation. The difference between baseline and maximum flows was used for calculation of percentage of blood flow increase. Because a relatively small sample was studied and because the data were calculated as percentages rather than absolute numbers, a normal distribution was not expected. The Kolmogorov- Smirnov test results confirmed this assumption. Therefore, nonparametric procedures were used for data analysis. The Wilcoxon matched pairs test was used for comparison of the different stimuli within the study samples. The Mann- .1 Natro- Oplillialmol, Vol. 18, No. 4, 1998 VISUALLY INDUCED REACTIVITY IN CEREBRAL BLOOD FLOW 265 Whitney test was applied to compare the same stimuli among the different groups. The data are expressed as mean percentage increase ± standard deviation. RESULTS Control Subjects In the control subjects, baseline blood flow of the PCA was 34.2 ± 6.4 cm/ sec in the older subjects and 38.0 ± 5.5 cm/ s in the young subjects. This difference was not significant. The young and elder normal subjects also showed no significant differences in VIR, visual imagery task and CO, tests. As a result, they were treated as one group for further evaluations ( Table 1). The on- off light stimulus increased blood flow velocities by 20.4 ± 5.9% in the left and by 22.5 ± 6.9% in the right PCA. Colored light increased blood flow velocities by 20.6 ± 6.8% on the left and by 23.9 ± 5.8% on the right side. There was no significant difference between these stimuli ( j? > 0.05). Complex scenes produced a significantly higher increase in blood flow velocity of 28.9% ± 6.7% in the right and 28.6 ± 6.9% in the left PCA ( p < 0.05) compared with increases with on- off light and colored light. Visual imagery had no significant effect on PCA flow velocities, compared with non- visually induced fluctuations of blood flow during the resting phase. In response to flow velocity with the imagined scene, there was either a slight increase or no change in blood flow velocity. Stimulation with C02 increased PCA blood flow velocities by 58.3 ± 9.5%. There was no significant difference between the right or left PCA. Patients With PCA Territory Infarctions In patients with PCA territory infarctions, baseline flow velocities on the affected side did not differ from values on the nonaffected side ( Table 2). In patients with complete homonymous hemianopsia, no significant VIR could be measured on the affected side ( Table 2). There was only one exception, a 77- year- old patient with a right- side PCA territory infarction and complete homonymous hemianopsia. In this patient, VIR to all stimuli on the affected side was comparable to that on the non-affected side. As in the control groups, visual imagery produced no significant increase on either side. In these patients C02 reactivity of the affected PCA was reduced to 30.4 ± 12.5%, which was 50% of the normal response on the nonaffected side. Patients with quadrantanopsia showed a reduced VIR only with the first two stimuli, compared with VIR in the nonaffected side ( p < 0.05), where C02 reactivity was reduced to 39.6 ± 20.1%, which corresponds to a reduction of 26.5% compared with the normal response. A summary of the results is shown in Figure 1. DISCUSSION Functional activation of the brain is coupled with a local increase in cerebral blood flow ( 14- 16), which is probably metabolically mediated by adenosine, K+ and H+ ( 9). We investigated VIR of normal control subjects and patients with occipital lobe infarction and found in normal subjects an association between the increase in blood flow velocity and the complexity of the visual stimulus. In patients with PCA territory infarction, however, we found significantly reduced reactivity, corresponding to the extent of brain damage: The more extensive the tissue damage, the greater the reduction in VIR and C02 vasomotor reactivity. There was no reaction to visual imagery in control subjects or patients with PCA territory infarctions. In positron emission tomography studies, Phelps and Mazziotta ( 2) and Phelps et al. ( 3) reported an increase in brain glucose metabolism in the primary visual cortex ( PVC) and in the visual association cortex in response to differing complexities of the visual stimuli. Our findings based on TCD measurements were, in principle, the same. The complex scene stimulus significantly increased flow velocity more than did the color and on- off light stimuli. This has been shown by the TCD study of Conrad and Kingelhofer ( 17) who also found a significant increase in blood flow velocity in the PCA after complex visual stimulation. Sitzer el al. ( 18) found an increase in blood flow velocity that was comparable to our results ( 30.4 ± 6.4%) in the PCA using TCD while showing a complex color video film. This can be explained by the lower informational content of the simple light and color stimuli. These stimuli should therefore mainly activate the PVC, whereas complex stimuli ( containing much information about shapes, perspective, or meaning of a scene) additionally activate the association cortex. Because TCD- VIR measurement of the PCA involves insonation of the PCA main branch, activating both the primary visual cortex and the visual association cortex, these vessels cannot be investigated separately. Phelps and Mazziotta ( 2), however, reported an increase in glucose metabolism of 12% in the PVC and an in- TABLE 1. Conlrols: baseline flow ( cm/ s), mean percent increase in blood flow velocity (%) and standard deviations in response to various stimuli in normal subjects iascline flow On- off light (%) Color (%) Complex scene (%) Visual imagery (%) CO, 4est (%) Right PCA Left PCA 35.5 ± 6.4 36.5 ± 6.0 22.5 ± 6.9 20.4 + 5.9 23.9 ± 5.8 20.6 ± 6.8 28.9 ± 6.7 * 3 ** 2 28.6 ± 6.9 ** 2 and 3 4.7 ± 6.7 4.2 ± 6.4 58.3 ± 9.3 57.3 ± 12.0 PCA, posterior cerebral artery. ** 2 = p < 0.05 compared with on- off light; * 3 = p < 0.05 compared with color, ** 2 and 3 = p < 0.01 compared with on- off light and color. ,/ Neiim- Ophthalnml. Vol. IK No. 4. I99K 266 B. SPELSBERG ET AL. TABLE 2. Patients with PCA territory infarctions: baseline flow ( cm/ s), mean percent increase in blood flow velocity (%) and standard deviations of the affected and. nonaffected PCA in response to various stimuli Quadrant- anopics Hemi- anopics AITecled PCA NonalTeclcd PCA AITecled PCA NonaiTcctcd PCA Baseline flow ( cm/ s) 27.7 ± 10.3 33.6 ± 10.2 35.0 ± 13.6 33.6 ± 8.3 On- off light (%) 11.1 ± 5.5* 21.3 + 8.2 3.8 ± 6.4** 18.6 ± 5.9 Color (%) 15.8 ± 8.4* 27.1 ± 5.9 0.9 ± 3.0** 21.9 ± 5.7 Complex scene (%) 22.4 ± 12.0 25.3 ± 4.3 2.7 ± 5.8** 32.6 ± 7.1 Visual imagery (%) 1.3 ± 2.4 4.2 ± 5.7 1.0 ± 3.2 4.7 ± 7.4 C02- tcst (%) 39.6 ± 20.1* 53.9 ± 15.4 30.4 ± 12.5** 59.6 ± 14.2 PCA, posterior cerebral artery. * = p < 0.05, ** = p < 0.01 compared wit the nonaffected side. crease of 6% in visual association cortex in response to white light, whereas a complex scene produced an increase of 45% in PVC and 59% in visual association cortex. Among our control subjects, no age- dependent differences in VIR were noted, a finding consistent with reports by Dastur et al. ( 19) and Gur et al. ( 20) Dastur et al. found no difference in brain 0 2 metabolism and blood flow in healthy young ( mean age, 21 years) subjects or elderly ( mean age, 71 years) subjects. In contrast, in another group of elderly subjects ( mean age, 73 years), even slight atherosclerotic alteration of the brain vessels significantly lowered blood flow. They concluded that elderly people with no cerebrovascular alteration have the same capacity for blood flow regulation as young people. In the control subjects, we found no significant difference in VIR between the left and right PCA, except for the reaction to the colored slide, which increased blood flow velocity more in the right PCA than in the left PCA. These results are in contrast to a TCD study of Harders et al. ( 21) who found a significantly higher VIR to all visual stimuli on the right side when projecting to visual hemifields. We did not project the visual stimuli to the two visual hemifields separately, which may explain the discrepancy between our findings and those of Harders et al. Visual imagery did not produce an increase in PCA flow velocity. On the contrary, in many subjects blood flow velocity slightly decreased, probably because of an activation of neighboring cortical areas during the task. With single photon emission computed tomogragphic l i i fS Light • Colour • Complex scene EJVisual imagery E3C02 CONTROLS FIG. 1. Percent change of posterior cerebral artery in flow in normal subjects and patients with posterior cerebral artery infarction due to various stimuli. studies, Goldenberg et al. ( 10- 13) identified a region in the left inferior temporal- occipital cortex that was activated specifically during visual imagery tasks. An explanation for the failure to detect a flow velocity increase in the PCA during the imagery task could be that visual imagery, as a modality of specific memory tasks, mainly activates temporolimbic structures that are supplied by the temporal branches of the MCA. Urban et al. ( 7) showed that the reduced VIR in response to photic stimulation in patients with occipital lobe infarction depends on the extent of damaged brain tissue. In support of their findings, in this study we found that patients with PCA territory infarctions had normal baseline flow velocities and reduced VIR values. The residual VIR was significantly less in patients with complete homonymous hemianopsia than in patients with quadrantanopsia. Whereas Urban et al. ( 7) stimulated subjects with flashed light only, we stimulated patients with complex stimuli and could show that patients with quadrantanopia patients had normal VIR after complex scene stimulation, indicating a sparing of association cortex in these patients. We conclude that there is a direct correlation between VIR and the extent of nonaffected PVC in patients with circumscribed PCA territory infarctions. Furthermore, we are the first to investigate C02 - induced vasomotor reactivity in the PCA, its relation to the extent of PCA territory infarction, and its relation to VIR. This question is of special interest because C 0 2 and visual stimulation involve different mechanisms: C02 leads to dilation of the arterioles directly, whereas VIR is dependent on neuronal activation and is probably mediated metabolically by K+, H+ and adenosine ( 9). After stroke, C02 reactivity is reduced because of dilated arterioles in the penumbra of the ischemic lesion, especially in patients with infarction due to internal carotid artery occlusion ( 22). Some investigators ( 23,24) have shown that the C02 vasomotor reserve in patients with PCA territory infarctions was not reduced when insonat-ing the basilar artery and have thereby concluded that these infarctions were caused by embolism. This was in line with Weiller et al. ( 25) who demonstrated no C02 reserve decrease in patients with cardiac embolic infarction of the middle cerebral artery. In contrast, our data show that C02 reactivity is reduced to a degree that corresponds to the extent of the PCA territory infarction, although PCA territory infarctions are known to be caused embolically. Until now, there are no data about ./ Neuro- Oplillmlmol, Vol. IX. No. 4, 1998 VISUALLY INDUCED REACTIVITY IN CEREBRAL BLOOD FLOW 267 C02 reactivity in the PCAs of patients with PCA territory infarctions. It is interesting that our patients showed a correlation between the extent of PCA infarction and the reduction in C02 reactivity. We are the first to show that reduced VIR to simple and complex stimuli resulting from decreased functional activation and reduction in C02 reactivity in patients with PCA territory infarctions occur in parallel. Patients with hemianopsia due to PCA territory infarction sometimes are severely impaired in coping with daily activities because of visual field deficits. In the rehabilitation of these patients, visual hemifield training using electronic devices helps to correct visual deficits to some degree ( 26,27). 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