Photoreactive Flow Changes in the Posterior Cerebral Artery in Control Subjects and Patients With Occipital Lobe Infarction
Background and Purpose Photoreactive flow changes of the posterior cerebral artery (PCA) in control subjects and patients with unilateral occipital lobe infarction were investigated to study the hypothesis that occipital lobe infarction of varying extent leads to a reduced visually activated flow increase in the ipsilateral PCA.
Methods Maximum mean flow velocity (MFV) of the PCA was investigated by transcranial Doppler sonography after photic stimulation of the retina.
Results In 25 control subjects MFV was increased by 30.6±9.7%. In 13 patients with unilateral occipital lobe infarction the ipsilateral MFV increase was significantly lower than in control subjects. Nine patients with homonymous hemianopsia showed an ipsilateral MFV increase of 3.4±4.1% (P<.001) and four patients with incomplete occipital lobe infarction and homonymous quadrantanopsia had an MFV increase of 16.0±12.8% (P<.05).
Conclusions We conclude that photoreactive flow changes of the PCA represent a noninvasive and reliable measure of functional impairment due to occipital infarction.
Aaslid1 first described blood flow velocity changes by TCD in the PCA under visual stimulation. In the present study, photoreactive flow changes of the PCA and MCAs in control subjects and patients with unilateral occipital lobe infarction were investigated to study the hypothesis that occipital lobe infarction of varying extent leads to a reduced visually activated flow increase in the ipsilateral PCA.
Subjects and Methods
The MFVs of both PCAs (P2 segment) and MCAs were measured with a transcranial 2-MHz pulsed Doppler device (Medasonics II) in 25 healthy volunteers and 13 consecutive patients with unilateral occipital lobe infarction (10 left, 3 right). In 1 additional healthy subject and 2 additional patients we attained no reliable Doppler signal because of an insufficient ultrasonic bone window. MFV was calculated by spectral analysis with fast Fourier transformation. All measurements were performed in a dark, silent room while each subject’s eyes were closed. After an adaptation period of 10 minutes and immediately before stimulation onset, the mean of three consecutive MFV measurements per second was calculated and taken as the base. Photic stimulation was performed with a strobe lamp placed at a distance of 0.3 m in front of the subjects. Flash light stimuli (duration, 10 μs/flash; power, 0.7 J/flash; Strobotest II) at a continuously increasing frequency from 1 to 20 Hz were applied over a period of 10 seconds. Immediately after stimulation each subject was asked to close his or her eyes. Maximal and minimal MFV values were documented, and the percent maximum increase (Δ1) and percent maximum decrease (Δ2) during and after photic stimulation were calculated. The sequence of insonation (PCA or MCA, left or right side) had no influence on the results. The structural and functional deficits were established in all patients on the basis of cranial CT or MRI and static Humphrey perimetry. Student’s paired t test and the Mann-Whitney-Wilcoxon U test were applied for statistical analysis.
Prestimulus MFV values for the PCA (Fig 1⇓) in control subjects were 35.6±6.0 cm/s and 36.7±5.8 cm/s on the right and left side, respectively. The MFV increased (Δ1) by 30.6±9.7% during photic stimulation and in the poststimulus period decreased (Δ2) by 33.6±11.2% to values slightly below the base. Differences between Δ1 and Δ2 and between the left and right PCA were not statistically significant.
In the 13 patients with unilateral occipital lobe infarction, the PCA showed normal Doppler spectra, and the prestimulus MFV values of the affected PCA (31.1±12.6 cm/s) and the unaffected side (30.8±10.1 cm/s) were not significantly different. Δ1 and Δ2 of the unaffected PCA were not significantly different from the control values.
In the affected PCA of 9 patients with homonymous hemianopsia due to occipital lobe infarction, visual stimulation induced only a small flow increase (Δ1, 3.4±4.1%) (Table⇓). This increase was significantly lower (P<.001) compared with the unaffected side and control subjects. In 4 patients with partial occipital lobe infarction and homonymous quadrantanopsia (2 each of the upper and lower visual hemifields), the evoked flow increase (Δ1, 16.0±12.8%) was significantly higher (P<.05) than that in the hemianoptic patients but less than that in control subjects (Table⇓).
In the MCA territory (Fig 2⇓), the MFV increase during flash light stimulation (Δ1) of control subjects and patients (n=13) was 7.1±8.9% and 3.0±5.2%, respectively, and the poststimulus decrease (Δ2) was 6.3±9.0% and 4.1±6.0%, respectively. In 1 patient with hemianopsia, the macular region of the visual field defect was spared but Δ1 (5%) and Δ2 (8%) of the ipsilateral MCA were in the same range as in the MCA of the 8 patients with hemianopsia and macular involvement (ipsilateral MCA Δ1, 5.5±3.9%; Δ2, 5.5±2.4%). The differences between control subjects and patients and between the left and right MCAs of either group were not statistically significant.
Cerebral blood flow is coupled with brain metabolism and brain function.2 Functional mapping studies with positron emission tomography3 and MRI techniques4 showed a localized increase in blood volume in the primary visual cortex during photic stimulation. Both methods have a low temporal resolution and limitations in quantifying the degree of functional activation.5 TCD allows on-line monitoring of blood flow changes. The relationship between blood flow velocity and blood volume within the large basal intracranial arteries is linear if alterations of the cerebrovascular bed are restricted to the small cortical resistance vessels.6 TCD studies have shown that changes in the diameter of the large basal arteries are negligible and intraindividual changes in blood flow velocity reflect changes in volume flow.6 7 8
Photic stimulation induces a marked MFV increase in the PCA of healthy subjects. Optimum differentiation between control subjects and patients is achieved by administering intermittent light stimuli with a strobe lamp. Stimuli frequencies ranging from 10 to 20 Hz have been shown to be most effective.9 The maximum flow increase (30.6±9.7%) was similar to that reported by Conrad and Klingelhöfer,10 who used 10 Hz–checkerboard stimulation (30.9±7.2%) and by Sitzer et al,11 who showed a color video film (30.4±6.4%). Aaslid1 obtained lower values by use of a whole-screen white-dark change causing an on-off stimulus (16.4±1.5%). In the present study, the MFV during photic stimulation rose steeply, reached a maximum flow increase that was followed by a slight decrease, and continued as a plateaulike velocity response. Thus, the maximum flow increase comprises an initial “overshooting” due to autoregulative mechanisms.10 The subsequent MFV decrease to the “working level” is explained by adaptation mechanisms of the retina and the visual cortex.1
PCA lesions causing visual field defects significantly reduce the MFV increase on the affected side during visual stimulation. The residual MFV reactivity was considerably less in patients with complete homonymous hemianopsia than in patients with quadrantanopsia. The differences between the three groups (control subjects and patients with quadrantanopsia and hemianopsia) were statistically significant. We feel that impairment of photoreactive flow changes in the PCA is a semiquantitative measure of the visual field defect. With flashlight stimulation, the flow response is independent of the patient’s cooperation.
In 8 of 9 patients with complete unilateral occipital lobe infarction, perimetry demonstrated that the homonymous hemianopsia also involved the macular region. Therefore, the small MCA flow increase found ipsilateral to the affected side cannot be explained by sparing of the occipital pole, the blood supply of which is derived from MCA branches in about 10% of subjects.12 As do Droste et al,13 we suggest that the small bilateral MCA flow increase is due to unspecific effects such as increased attention and arousal evoked by photic stimulation.
Selected Abbreviations and Acronyms
|MCA||=||middle cerebral artery|
|MFV||=||mean flow velocity|
|PCA||=||posterior cerebral artery|
|TCD||=||transcranial Doppler sonography|
- Received May 11, 1995.
- Revision received June 30, 1995.
- Accepted July 3, 1995.
- Copyright © 1995 by American Heart Association
Aaslid R. Visually evoked dynamic blood flow responses of the human cerebral circulation. Stroke. 1987;18:771-775.
Sokoloff L. Relationship among local functional activity, energy metabolism, and blood flow in the central nervous system. Fed Proc. 1983;40:2311-2316.
Phelps ME, Mazziotta JC, Kuhl DE, Nuwer M, Packwood J, Metter J, Engel J. Tomographic mapping of human cerebral metabolism: visual stimulation and deprivation. Neurology. 1981;31:517-529.
Belliveau JW, Kennedy DN, McKinstry RC, Buchbinder BR, Weisskoff RM, Cohen MS, Vevea JM, Brady TJ, Rosen BR. Functional mapping of the human visual cortex by magnetic resonance imaging. Science. 1991;254:716-719.
Bishop CCR, Powell S, Rutt D, Browse NL. Transcranial Doppler measurement of middle cerebral artery blood flow velocity: a validation study. Stroke. 1986;17:913-915.
Gomez SM, Gomez CR, Hall IS. Transcranial Doppler ultrasonographic assessment of intermittent light stimulation at different frequencies. Stroke. 1990;21:1746-1748.
Sitzer M, Diehl RR, Hennerici M. Visually evoked cerebral blood flow responses. J Neuroimaging. 1992;2:65-70.
Droste DW, Harders AG, Rastogi E. A transcranial Doppler study of blood flow velocity in the middle cerebral arteries performed at rest and during mental activities. Stroke. 1989;20:1005-1011.