Neuroradiology

Posterior Cerebral Artery Occlusion: Clinical, Computed Tomographic, and Angiographic Correlation 1 Katsuya Goto, M.D., 2 Koichi Tagawa, M.D., Kazuo Uemura, M.D., Kiyoshi Ishii, M.D., and Shoki Takahashi, M.D.

The distribution of low-density areas on computed tomography (CT) suggested occlusions in the proximal half of the circummesencephalic portion in 38 patients with posterior cerebral artery (PCA) occlusion. Correlation between clinical, CT, and angiographic findings in 24 cases showed that occlusion was most common in the crural segment. Clinical manifestations and infarction extension varied widely among proximal occlusions. In cases with good collateral filling, the infarction was restricted to the thalamus; in those with poor filling, it involved most of the PCA's territory, and hemorrhagic transformation occasionally ensued. Discrepancies between findings were ascribed to dislodging of emboli or thrombi, recanalization, and transient obscuration of the infarction on CT. INDEX TERMS: Arteries, cerebral. Brain, infarction. Cerebral blood vessels, angiography. Cerebral blood vessels, stenosis • Computed tomography, head, 1[0] .1211 • (Cerebral vessel, low flow state, 1[7] .760) • (Cerebral vessel, embolus, 1[7].770). (Posterior cerebral artery, low flow state, 1[756].760) Radiology 132:357-368, August 1979

manifestations of posterior cerebral artery (PCA) occlusion range from midbrain syndromes to thalamic syndromes and disturbances in cortical and higher cortical functions of the temporal and occipital lobes. However, little is known as to why a thalamic syndrome develops in one case, a disturbance in higher cortical function in another, and a combination of these two in still another case. No study of this problem from a neuroradiological viewpoint has been made, and only sporadic case reports (3,4,8, 13, 17)had been issued until recently, when Einsiedel-Lechtape et al. (6) made extensive angiographic studies on 27 patients with PCA occlusion. However, as has been stated, "angiographic attempts to demonstrate occlusions of the PCA or its branches frequently fail to provide satisfactory correlation with clinical findings" (14). Computed tomography (CT) gave us a new approach to the understanding of the precise localization

and sequential changes of infarction. This report deals with a comparison of clinical features, distribution of lowdensity areas on CT, and occlusive changes in the PCA on angiography. It uses these to investigate infarction in the PCA territory in relation to the development of collaterals, dislodging of thrombi or emboli, recanalization, and hemorrhagic transformation.

C

LINICAL

TABLE I:

PATIENTS AND METHODS

In a consecutive series of about 2,700 patients who underwent CT examination from August 1976 to August 1978, CT diagnosis of cerebral infarction was made in 450. A clinical and CT diagnosis of PCA occlusion was made in 38 of these. The distribution and extent of low-density areas on CT were compared with the territories of the PCA. CT scans were obtained without angulation against the

CT DISTRIBUTION OF INFARCTION IN 38 CASES OF CUNICALL Y SUSPECTED PCA OCCLUSION

PCA Occlusion

4 Patients without PCA occlusion

2 3 1 3 1 2

0 0 1 0 0 1

5 3

2 0

20 Patients with Distribution of Infarct on CT Thalamus Thalamus Occipital Thalamus Occipital Post. Temporal Thalamus Occipital Post. Temporal Post. Parietal Occipital Post. Temporal Occipital Post. Temporal Occipital Post. Temporal Post. Parietal

+ + +

+ +

+ +

+

+

14 Patients without Verification by Vertebral Angiography

1

o 1 2

Total

3 3 3 5 4 6

3 3 4

11

o

3

1 From the Division of Radiological Sciences (K.G., K.U., K.!., S.T.) and Division of Neurology (K.T.) of the Research Institute of Brain and Blood Vessels, Akita, Japan. Received Nov. 7, 1978; accepted March 2, 1979. 2 Present address: Department of Radiology, School of Medicine, Fukuoka University, Nanakuma, Fukuoka-shi 814, Japan. jr

357

=

=

Occlusion Occlusion Occlusion Occlusion Occlusion Stenosis Stenosis Occlusion -recanalization Occlusion -recanalization Occlusion -recanalization (R)

Occlusion Occlusion Occlusion

Crural

11:

Ambient

Occlusion -recanalization (l) Stenosis(BIL) Occlusion Occlusion Stenosis Stenosis

PCA

Occlusion Occlusion Occlusion

Occlusion(BIL)

Stenosis

Cortical Branches

Angiography

24

Stenosis Stenosis Stenosis Stenosis

None

None Poor Poor

None

Moderate

None Poor

Moderate Poor Moderate Moderate Good

Good Good Moderate Poor

Retrograde Filling of PCA

Infarction

Infarction

Infarction

Hemorrhagic infarction(R)

Infarction Infarction

Infarction

Infarction

Infarction Infarction

Thalamus

Posterior Temporal

Infarction Infarction Infarction Infarction Infarction Infarction Hemorrhagic infarction

Infarction Hemorrhagic infarction

CT

Infarction Hemorrhagic infarction

Infarction

Infarction

Posterior Parietal

Infarction Infarction Infarction Hemorrhagic infarction

Infarction(Bll) Infarction Infarction Infarction Infarction

Infarction Infarction Infarction Infarction Infarction Hemorrhagic infarction

Infarction

Infarction(BIL)

Hemorrhagic infarction

Infarction(Bll) Infarction

Hemorrhagic Hemorrhagic Hemorrhagic infarction(Bll) infarction(Bll) infarction(Bll)

Hemorrhagic infarction Infarction Infarction Infarction Infarction Infarction Infarction Infarction Hemorrhagic infarction Infarction

Occipital

CASES OF POSTERIOR CEREBRAL ARTERY OCCLUSION

Vertebral Basilar

ANGIOGRAPHy-CT CORRELATION OF

left; Bll bilateral. R = right; L Grading of retrograde filling of the PCA: All of the cortical branches of the PCA were visualized in the midarterial phase. and the trunk of the PCA was opacified back to the origin of the posterior temporal artery in the capillary Good phase. Poor = Only one or two of the cortical branches of the PCA showed delayed and faint opacification in the capillary phase.

15 16 17 18 19 20 21 22 23 24

14

13

6 7 8 9 10 11 12

=

Occlusion

1 2 3 4

5

Interpeduncular

Case No.

TABLE

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Cl.)

CD

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CD

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(J)

:0

m

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0 --i 0

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Fig. 1. CT,sca~s in CASE I. A small Iow-density lesion which was seen in the posterolateral part of left thalamus 7 days after onset (a) became obscure after infusion of contrast material (b). c. The lesion was no longer visible 17 days after onset. d. A discrete but smaller Iow-density lesion again became apparent 15 months after onset. F~g. 2. Vertebral angiogram .inCASE I shows complete occlusion of left PCA in the crural segment 7 days after onset. Fig. 3. Lateral (a) and AP (b) Images of left carotid angiogram in CASE I. late arterial phase, show good retrograde filling of the occluded PCA back to the proximal ambient segment (arrows).

orbitomeatalline using EMI scanner Model 1000 or Model 1010. CT-angiography correlation was made in 24 cases. Vertebral angiograms were obtained by selective cannulation of the vertebral arteries in most patients. However, retrograde brachial angiography was necessary in a few patients with severe arteriosclerosis. If vertebral angiography revealed PCA occlusion, carotid angiography was carried out on the same side for the evaluation of degree and extent of collateral filling of PCA branches from cortical branches of the middle and anterior cerebral arteries via leptomeningeal anastomoses. In a few cases with aplasia or severe hypoplasia of the horizontal portion of the anterior cerebral artery, carotid angiography of the contralateral side was added. Clinical manifestations, such as thalamic and occipital lobe syndromes, were evaluated neurologically, and correlation was made with the neuroradiological findings.

RESULTS

The distribution and extent of low-density areas seen on CT were tabulated for 38 patients (TABLE I). There were 14 patients who had involvement of the thalamus and 14 who demonstrated extensive low-density areas involving the posterior temporal and occipital lobes. The CT-angiographic correlation in 24 patients (TABLE 11) demonstrated a high incidence of proximal occlusion and showed the most common site of occlusion to be the crural segment. Various degrees of retrograde filling via leptomeningeal anastomoses with posterior branches of the middle cerebral artery were demonstrated in 13 out of 14 patients with proximal occlusion. Collateral flow to a branch of the PCA from the anterior cerebral artery was recognized in only 1 patient (Fig. 15). In 1 patient, no collateral filling of branches of an occluded PCA was demonstrated by carotid injection (Figs. 20 and 22). Relatively good correlation was

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Fig. 4. CT scans in CASE 11. a. A well circumscribed low-density lesion is seen in the anterior part of left thalamus 3 days after onset. b. Considerable obscuring of the lesion was noted 7 days after onset. c. The lesion became hardly recognizable at 15 days. d. A discrete but smaller low-density lesion became apparent again 5 months after onset. Fig. 5. Vertebral angiography in CASE 11 6 days after onset shows complete occlusion of left PCA in the interpeduncular segment (arrow). Fig. 6. a and b. Left carotid angiography in CASE 11, capillary phase, shows good retrograde filling of the occluded left PCA back to the proximal ambient segment (arrows).

seen between the distribution and extent of low-density areas on CT and the degree of retrograde filling in 10 out of 13 patients with proximal occlusion. In 2 cases with extremely good collateral filling, the low-density area was entirely restricted to the thalamus (Figs. 1 and 4). On the contrary, in 6 cases with poor or no detectable filling, the low-density area extended to almost the entire PCA territory (Fig. 12). Features of hemorrhagic infarction were seen in 3 of these cases. A considerable number of cases showed a discrepancy between CT and angiographical findings (TABLE 11). There were 3 cases of proximal occlusion (Patients 7-9) with extensive areas of decreased density on CT in spite of relatively good angiographic visualization of collateral filling of the occluded PGA. Also noted were 2 cases (Patients 16 and 18) with a discrepancy between the postulated site of occlusion as judged from the distribution and extent of the low-density area on CT and the actual site of

occlusive change demonstrated on angiography. In addition, there were 4 cases (Patients 21-24) with extensive areas of decreased density in spite of the absence of obvious PCA occlusion on angiography. In these cases, stenoses of varying degree were seen in the basilar artery or distal vertebral arteries and their infratentorial branches. CASE REPORTS CASE I (Patient 2 in TABLE 11): Following the acute occurrence of a cheiro-oral syndrome, this 59-year-old man developed a typical Dejerine-Roussy syndrome consisting of hemiparesis, hemihypesthesia, slight incoordination, and thalamic pain on the right side. CT 7 days after onset revealed a localized low-density area in the posterolateral part of the left thalamus (Fig. 1a). After infusion of contrast material, the lesion became considerably obscured (Fig. 1b) and became unrecognizable 17 days after onset (Fig. 1c). However, 15 months after onset, eT revealed a smaller but discrete area of decreased density (Fig. 1d).

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7,8a,8b

Fig. 7. CT scan in CASE "' 3 days after onset. CT was repeated 5 and 10 days after onset; however, no area with abnormal brain density could be seen in the thalamus though the patient presented with an apparent thalamic syndrome . . Fig. 8. AP (a) and lateral (b) magnification vertebral angiography in CASE Ill. The right PCA was occluded in the crural segment just distal to the junction with the posterior communicating artery (arrow in a). Poor opacification of the left PCA was due to abundant nonopacified blood from the left carotid system. There was good opacification of the anterior thalamoperforating artery (crossed arrows) and interpeduncular thalamoperforating arteries (double arrows). Fig. 9. Right carotid angiography in CASE Ill, capillary phase, shows good retrograde filling. of the occluded PCA back to the proximal ambient segment (arrows in b).

Vertebral angiography 4 days after onset revealed an occlusion of the left PCA in the crural segment (Fig. 2). Carotid angiography showed excellent opacification of the left PCA in retrograde fashion back to the proximal ambient segment via leptomeningeal anastomoses between cortical branches of the occluded PCA and those of the middle cerebral artery (Fig. 3). The hospital course was relatively favorable and the patient was discharged 5 weeks after onset with a thalamic hand deformity and thalamic pain on the right side. CASE 11 (Patient 1 in TABLE 11): This 58-year-old woman presented with memory disturbance, hemihypesthesia, hemiparesis, thalamic pain, incoordination and homonymous hemianopsia on the right, and Homer syndrome on the left. CT 3 days after onset revealed a well circumscribed low-density area in the anterior part of the thalamus on the left (Fig. 4a). Repeat CT 7 days after onset demonstrated a considerable increase in absorption coefficient of this lesion, with blurring of the margin (Fig. 4b). The lesion became hardly recognizable 15 days after onset (Fig. 4c). However, follow-up CT after 5 months again revealed a smaller and well circumscribed area (Fig. 4d). Vertebral angiography 6 days after onset demonstrated complete occlusion of the left PCA a few millimeters distal to its origin (Fig. 5). Carotid angiography showed good filling of the cortical branches and trunk back to the proximal ambient segment (Fig. 6). The hospital course was good and the patient was discharged 50 days after onset with only thalamic pain and right homonymous hemianopsia persisting. CASE III (Patient 7 in TABLE 11): This 54-year·old man had been hy-

9a,b

pertensive since his late thirties. The day before admission, he was awakened by a severe headache. He complained of dizziness, walked unsteadily and tended to fall to the left. On admission, he complained of paresthesia over the left half of his lips. Neurological abnormalities included prominent incoordination, slight hemiparesis, slight hemihypesthesia to touch and pain, and homonymous hemianopsia on the left. Also noted was a right Homer syndrome. CT performed 3, 5, and 10 days after onset showed no abnormality in brain density either in the thalamic region or the occipital lobe on the right (Fig. 7). The right PCA was occluded in the crural segment just distal to the junction with the posterior communicating artery. There was good opacification of the anterior and interpeduncular thalamoperforating arteries (Fig. 8). Carotid angiography revealed good retrograde filling of the cortical branches and trunk back to the proximal ambient segment (Fig. 9). The patient's hospital course was excellent, and he was discharged after one month, with only slight hemiparesis on the left. CASE IV (Patient 18 in TABLE 11): This 71.year-old hypertensive man had had episodes of mild heart failure every 2 to 3 months for the previous 4 years. The last episode occurred one week prior to admission; 3 days prior to admission he developed an acute sensory disturbance over the right half of his body. Neuroloqical examination on admission revealed slight hemihypesthesia to touch and pain, and homonymous hemianopsia on the right. CT 3 days after onset showed a small vaguely delineated low-density lesion in the posterolateral part of the left thalamus and medial aspect of the left occipital lobe (Fig. 10). Vertebral angiography at 11 days revealed a conspicuous filling defect suggestive

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10, 11

Fig. 10. CT scan in CASE IV 3 days after onset shows small, lowdensity areas in the posterolateral portion of the thalamus and medial occipital lobe on the left. Fig. 11. Vertebral angiogram in CASE IV 11 days after onset shows a marked filling defect, probably by embolus, in the ambient segment of the left PCA (arrows).

of an embolus in the ambient segment just distal to the origin of. the posterior temporal artery (Fig. 11, arrows). In addition, there was nonopacification of the calcarine artery, which is usually a branch of this segment of the artery. Carotid angiography was unremarkable without retrograde filling of the occluded cortical branches. CASE V (Patient 12 in TABLE 11): .This 53-year-old man had had several attacks of vertigo for 2 months. Two days prior to admission, he began to have episodes of a sparkling sensation in his visual field. One day prior to admission, he complained of blurred vision and paresthesia over the right half of his body. Abnormal neurological findings on admission included a considerable memory disturbance, homonymous hemianopsia, slight disturbance in touch and position sensation, and slight hemiparesis on the right side. Also noted was a right Horner syndrome. CT 2 days after onset revealed an extensive area of decreased density which extended from the posterior temporal lobe to almost the entire occipital lobe on the right. Two small low-density areas were also seen in the posterolateral portion of the thalamus and in the middle of the posterior limb of the internal capsule (Fig. 12a). Vertebral angiography 3 days after onset revealed complete occlusion of the right PCA in the crural segment (Fig. 13). Retrograde filling by right carotid injection was poor, and only a branch of the posterior temporal artery was faintly opacified (Fig. 14b, arrows). This seemed related to poor filling of temporal branches of the middle cerebral artery (Fig. 14a). The anterior cerebral arteries were opacified bilaterally by left carotid injection, as there was aplasia of the horizontal portion of the anterior cerebral artery on the right side. There was also a faint retrograde filling of the parieto-occipital branch of the PCA via the leptomeningeal anastomosis, with the inferior internal parietal branch of the anterior cerebral artery in the late arterial phase (Fig. 15). Follow-up CT at 9 days showed further decrease in the absorption

coefficient of the infarcted area (Fig. 12b). However, CT at 25 days showed a marked increase in absorption coefficient, with obscuration of the entire lesion (Fig. 12c). There were some patchy areas of slightly increased density within the lesion; these showed some staining upon contrast enhancement. Follow-up vertebral angiography 27 days after onset showed recanalization. However, there still was a considerable luminal narrowing in the ambient segment and marked delay in circulation in the distal trunk and its cortical branches (Fig. 16). Gradual improvement of the neurological deficits occurred without remarkable change in the clinical course in association with recanalization; the patient was discharged 42 days after onset with persisting left homonymous hemianopsia. CASE VI (Patient 16 in TABLE 11): This 61-year-old man had been hypertensive since his late twenties. Two days prior to admission, he complained of paresthesia in his right hand. A few hours later he became somewhat delirious. Neurological examination on admission revealed memory disturbance, pure alexia (alexia without agraphia), and right homonymous hemianopsia. Vertebral angiography 9 days after onset revealed complete occlusion of the left PCA in the ambient segment just proximal to the origin of the posterior temporal artery (Fig. 17). Only the parieto-occipital artery was opacified in retrograde fashion by left carotid injection (Fig. 18, arrows). CT 1 month after onset demonstrated a large area of decreased density extending from the occipital lobe to the posterior parietal lobe on the left (Fig. 19). A small area of decreased density was also seen in the thalamus on the left. The patient was re-examined after one year; he had recovered considerably from the pure alexia. CASE VII (Patient 14 in TABLE 11): This 71-year-old hypertensive man often had palpitations for the last 17 years. Fourteen days prior to ad-

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12c,13

14a,b

Fig. 12. CT scans in CASE V. a. An extensive low-density area is present in almost the entire territory of the right PGA, including the thalamus, 2 days after onset. b. There is increased prominence of the lesion with reduction of absorption coefficient 9 days after onset. c. Decreased prominence of the lesion with marked increase in absorption coefficient in the low-density area 25 days after onset suggests recanalization. Fig. 13. Vertebral angiogram in CASE V 3 days after onset shows occlusion of the right PCA in the crural segment. Fig. 14. Arterial phase (a) and capillary phase (b) of right carotid angiogram. There was a marked luminal narrowing of the internal carotid artery both in the cavernous and supraclinoid portions (arrows in a). Poor filling of the temporal branches (crossed arrows in a) was due to marked stenosis in the proximal portion of the posterior trunk of the middle cerebral artery. There was a faint retrograde opacification of some branches of the posterior temporal artery (arrows in b). The anterior cerebral artery was not seen, due to aplasia of its horizontal portion.

mission, he noticed a visual disturbance and had difficulty reading. Neurological examination on admission revealed pure alexia, color agnosia, and right homonymous hemianopsia. Vertebral angiography

20 days after onset showed complete occlusion of the left PCA in the middle of the ambient segment (Fig. 20). Carotid angiography did not reveal any collaterals to the cortical branches (Fig. 21). Moderate-to-

KATSUYA GOTO AND OTHERS

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15,16

Fig. 15. Leftcarotid angiogram in GASE V, capillary phase. Bilateral anterior cerebral arteries were opacified by left carotid injection. There was faint retrograde filling of the parieto-occipital artery onthe right (arrows). Fig. 16. Follow-up vertebral angiogram in GASE V 27 days afteronset shows recanalization of the right peA.There was marked luminal narrowing inthecrural and ambient segments (arrows) and a marked delay in filling of the parieto-occipital and calcarine branches (crossed arrows).

marked arteriosclerotic changes were obvious in the internal carotid artery and its branches generally. The patient was discharged 70days after onset without remarkable change in hisalexic syndrome. One morning, 10months afterthefirstattack, thepatient was found to beconfused and hemiparetic ontheright. Neurological examination onadmission revealed cortical blindness and Anton syndrome (denial of blindness). Also noted was a slight hemiparesis and hemihypesthesia on the left. Vertebral angiography 4 days after the second attack demonstrated almost complete occlusion of theright PGA in its crural segment. On theother hand, there was complete recanalization of the left PGA with good opacification of its cortical branches (Fig. 22). Once again, carotid angiography didnotreveal any recognizable collaterals to the PGA territory ontheright (Fig. 23). A considerable tortuosity in the internal carotid artery and its branches and moderate stenosis in the initial segment and cavernous portion were noted. C'I performed 8 days after the second attack showed a poorly demarcated area of slightly decreased density in almost the entire territory of thePGA on theright side (Fig. 24a). Follow-up GT at 13days demonstrated patchy high-density areas scattered inthelesion (Fig. 24b). Upon contrast, the entire territory of the PGA was stained densely ontheright (Fig. 24c). Also noted was a well circumscribed area of markedly decreased density occupying the entire territory of the left PGA. This lesion had shown similar sequential changes to those seen ontheright side after thefirstattack. The patient was discharged 61 days after onset without remarkable change in the cortical blindness and Anton syndrome. DISCUSSION CT and vertebral angiography showed that the incidence of PCA occlusion in the proximal half of the circurnmesencephalic portion was relatively high. However, the extent of infarction varied considerably. In cases with good collateral filling, all of the cortical branches of the PGA were visualized in the midarterial phase in retrograde fashion, and the trunk was opacified back to the origin of the posterior temporal artery in the capillary phase. In 2 cases, a low-density area on CT was entirely restricted to

the thalamus (CASES I and 11). Most of the thalamus is supplied by many small branches off the posterior communicating artery and the proximal portion of the PCA (5, 7, 11, 12, 15, 18, 19). The anterior thalamoperforating arteries arise from the posterior communicating artery and supply the anterior nuclear group and the ventral anterior nucleus of the thalamus. The anterior nuclear group is considered to participate in autonomic nervous function. It is known that Homer syndrome occurs with lesions in the anterosuperior part of the thalamus. The posterior thalamoperforating arteries consist of the interpeduncular thalamoperforating branches and the thalamogeniculate perforating branches. The former supply the inferior part of the medial dorsal, ventral lateral, and ventral intermediate nuclei. The latter supply the medial portion of the lateral geniculate body, the anterior part of the ventral posterolateral nucleus, and the ventral posteromedial nucleus. The function of the medial dorsal nucleus is not well known, but it is considered that it plays some role in maintaining the level of consciousness, psychic activities, and autonomic nervous functions. Lesions in the ventral lateral and intermediate nuclei are considered to be pertinent to dystonia, hyperkinesia, and incoordination. The ventral posterolateral and posteromedial nuclei are terminal stations of the spinothalamic and trigeminal thalamic tract, respectively. The medial posterior choroidal artery gives off small branches to the dorsomedial nucleus. The lateral posterior choroidal artery gives off many twigs which supply the dorsomedial nucleus, pulvinar, and lateral geniculate body. One of the most well defined thalamic syndromes is Dejerine-Roussy syndrome, which consists of a disturbance in superficial and deep sensation, thalamic pain,

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19a

19b

Fig. 17. Vertebral angiogram in CASE VI9 days after onset. The left PCA was occluded in the ambient segment just proximal to the origin of the posterior temporal artery. Fig. 18. Left carotid angiogram, capillary phase. Only the parieto-occipital branch of the left PCA was opacified in retrograde fashion (arrows). Fig. 19. a and b. CT scans in CASE VI 1 month after onset. A small area of decreased density was seen in the thalamus, and a large area of decreased density extended from the occipital lobe to the posterior parietal lobe on the left side.

homonymous hemianopsia, slight hemiparesis, and slight ataxia of the contralateral side caused by occlusion of the thalamogeniculate arteries. Unilateral cerebellar ataxia with or without choreoathetoid movement is also well known to be caused by occlusion of interpeduncular thalamoperforatearteries. Even if there is good retrograde filling of the branches and trunk of the occluded PCA, perfusion pressure is considered to be lowest in the circummesencephalic portion just distal to the occlusion, where many feeders to the thalamus are given off. Therefore, some of the differences in the features of thalamic syndromes and in the appearance of low-density areas on CT in cases of proximal PCA occlusion might be due to differences in the site of occlusion and degree of collateral filling. In CASE I, the left PCA was occluded in the crural segment, but there was good retrograde filling of the cortical branches and trunk back to the proximal ambient segment. The low-density area on CT was relatively small and was restricted to the posterior lateral aspect of the thalamus. Clinical and neuroradiological findings suggested involvement of the ventral posterolateral and posteromedial nuclei of the thalamus by a circulatory disturbance in the thalamogeniculate perforating arteries. In CASE 11, the left PCA was occluded a few millimeters distal to its origin, but there was good retrograde filling of the cortical branches and trunk back to the proximal ambient segment. No opacification

of the posterior communicating artery and anterior thalamoperforating arteries was seen by left carotid injection. Thoughthe low-density lesion was restricted to the anterior part of the thalamus on CT, clinical findings suggested involvement of the ventral posterolateral and posteromedial nuclei, in addition to the anterior nuclear group, the medial dorsal and ventral lateral nuclei. Therefore, it was considered that there was circulatory disturbance both in the anterior and posterior thalamoperforating arteries. No area with abnormal brain density was seen in the midbrain of this patient. None of our patients with proximal PCA occlusion presented with the mesencephalic syndrome, and this might be attributed to a considerable potentiality of perforating arteries to develop collateral pathways between themselves before they penetrate the brain substance (10). In CASE Ill, vertebral angiography revealed occlusion of the right PCA just distal to the junction with the posterior communicating artery. Right carotid angiography demonstratedgood retrograde filling of the cortical branches and trunk of the PCA back to the proximal ambient segment. Neurological findings suggested involvement of the ventral lateral and intermediate nuclei which are supplied by the interpeduncular thalamoperforating arteries, in addition to the involvement of the anterior nucleus and the ventral posterolateral and posteromedial nuclei. Therefore, it was considered that an embolus seen in the proximal crural segment on vertebral angiography

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20,21

22,23

24a

24b

24c

POSTERIOR CEREBRAL ARTERY OCCLUSION

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had dislodged from the interpeduncular portion of the PCA. CT failed to reveal a thalamic infarct in spite of multiple attempts. In CASE IV, there was a marked narrowing in the distal ambient segment of the PCA with occlusion of the calcarine artery. However, CT revealed a smalllow-density area in the posterolateral portion of the thalamus as well as the medial aspect of the occipital lobe on the left. Clinical abnormalities included the thalamic syndrome as well as homonymous hemianopsia and an optic ataxia-like syndrome. Therefore, the embolus seen in the ambient segment was inltially considered to be located in the anterior half of the circummesencephalic portion. In Gases with proximal occlusion of the PCA with poor retrograde filling of the cortical branches and trunk, the area of decreased density was relatively extensive, involving almost the entire territory of the PCA. The cause of poor collateral filling of the occluded PCA and its branches was shown in most cases to be marked stenosis in one or mor~ of the following: the distal internal carotid artery, sphenbidal portion of the middle cerebral artery, and posterior' trunk of the middle cerebral- artery or its branches. In 3' cases (Patients 4, 12, and 14 from TABLE 11) with poor or absent collateral filling, follow-up CT showed features of hemorrhagic infarction. One of the present authors has noted with regard to infarction of the middle cerebral artery territory, that if recanalization occurs in the area perfused poorly by collaterals, the infarction tends to become hemorrhagic (16). In CASE V the PCA was occluded in the ambient segment, but there was only faint retrograde filling of some of the cortical branches of the PCA seen on the carotid angiogram. The low-density area on CT extended to involve the entire territory of the PCA. Complete recanalization occurred 27 days after onset, and hemorrhagic transformation of the infarction ensued. In .cASE VI, the PCA was occluded just before the origin of the posterior temporal artery, Only the parieto-occipital artery was opacified faintly on the carotid angiogram. CT showed a relatively extensive low-density area in the occipitat lobeand posterior parietal lobe. In CASE VII, bilateral occlusion of the proximal PCA, which occurred after a 10-month interval, caused' cortical blindness and Anton syndrome Collateral filling of the PGA and its branches were not seen on carotid angiogram on either side. Extensive areas of decreased density in the entire territory of the PCA later showed features of hemorrhagic infarction bilaterally'. Pure alexia was seen in 4 cases with rather extensive areas of infarction in the left occipital lobe. In 2 cases with relatively good opacification of the parieto-occipital artery e,

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Neuroradiology

either in antegrade or retrograde fashion, pure alexia was transient. However, in 2 cases with no collateral filling of this artery, it was severe and persistent. Little is known about the pathomechanism of pure alexia, mainly because of the rarity of autopsy cases. It has been considered that a lesion which involves the inferomedial aspect of the occipital lobe and splenium of the corpus callosum is pertinent to its development. However, it was suggested from a review of reports on 17 autopsy cases that involvement of the splenium of the corpus callosum is not indispensable for the development of pure alexia (2). It was also said that though it could occur without involvement of splenium, it was more severe and irreversible when the splenium was involved (9). The splenium of the corpus callosum is supplied by the posterior pericallosal artery. Though this artery was not identifiable in our patients, relatively good filling of parent arteries of this branch was noted in 2 patients who recovered considerably from pure alexia. Therefore it might be considered that good opacification of the parent arteries of the posterior pericallosal artery prevented extension of the infarction into the splenium. Cortical blindness caused by bilateral occlusion seems to be the most troublesome manifestation of PCA occlusion. Though this syndrome was seen in only 2 patients in this series, there were 3 others who had severe stenosis of the contralateral PCA. A considerable number of cases showed remarkable discrepancies between the findings of CT, angiography, and clinical presentation (TABLE 11). Three patients with proximal PCA occlusion (Patients 7 [CASE Ill], 8, and 9) showed a large area of infarction despite relatively good collateral filling. This might be due to systemic or local factors which hindered development of collaterals to the occluded PCA, which might have developed otherwise. In Patients 16 and 18 (CASES VI and IV, respectively) discrepancies in the findings of these two examinations were thought to be due to dislodging of a disintegrating embolus. In 4 patients (Patients 21-24) without PCA occlusion on angiography, complete recanalization seemed to have occurred following a relatively large infarction. In Patient 24 there were features of hemorrhagic infarction. Repeat vertebral angiograms showed recanalization in 3 other patients. CT does not always clearly reveal the area of infarction. Thalamic infarctions, which are usually quite small, sometimes become unrecognizable 2 to 3 weeks after onset, even when multiple overlapping scans are obtained (CASES I and 11). The pathomechanism which causes such transient obscuration of the infarcted area is

Fig. 20. Vertebral angiogram in CASE VII 20 days after onset. The left PCA was occluded in the middle of the ambient segment. Fig. 21. Left carotid angiogram in CASE VII, capillary phase, shows no retrograde filling of the occluded PCA. Fig. 22. Vertebral angiogram in CASE VII 4 days after the second attack. The right PCA was almost completely occluded in the crural segment, while the left PCA was completely recanalized. Fig. 23. Right carotid angiogram in CASE VII, capillary phase, shows no retrograde filling of the occluded PCA. Fig. 24. CT scans in CASE VII. a. A vaguely demarcated low-density area extended to almost the entire territory of the right PCA including the thalamus 8 days after the second attack. b. Patchy high-density areas appeared in the low-density lesion on the precontrast study 13 days after the second attack. c. There was dense staining in almost the entire territory of the right PCA after infusion of contrast material.

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obscure, but it might be due to the occurrence of a collateral blood supply from the surrounding normal area to the area of infarction where the blood-brain barrier is damaged. There was only 1 patient (CASE Ill) in whom repeated C'I failed to reveal thalamic infarction in spite of the obvious thalamic syndrome and PGA occlusion in the crural segment. Not infrequently, CT failed to reveal a sufficiently larqe lesion to account for the apparent disturbance of higher cortical function of the occipital lobe. This might imply that CT is not sensitive enough to detect areas of incomplete mfarctlon. It was also noted that eT diagnosis of infarcts became considerably more difficult when the absorption coefficient increased as a result of hemorrhagic transformation (CASES V and VII). Therefore it may be said that for the precise evaluation of the extent of infarction, a correlation of clinical, C'I, and angiographic findings is mandatory; discrepancies, however, are not exceptional. ACKNOWLEDGMENT: We wish to thank Drs. Christopher Willis and Kazutaka Toyonagafor reviewing the manuscript and Miss Shoko Ishioka for her secretarial assistance. Department of Radiology School of Medicine Fukuoka University Nanakuma, Fukuoka-shi 814 Japan

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August 1979

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