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(Stroke. 1995;26:131-136.)
© 1995 American Heart Association, Inc.

Articles

Progressive Cerebral Occlusive Disease After Radiation Therapy

M. Bitzer, MD H. Topka, MD

From the Departments of Neuroradiology (M.B.) and Neurology (H.T.), University of Tübingen (Germany).

Correspondence to Helge Topka, MD, Department of Neurology, University of Tübingen, Hoppe-Seyler-Str 3, 72076 Tübingen, Germany.

	Abstract

Top Abstract Introduction Case Report Review of the Literature Discussion References

 
Background A case of progressive irradiation-induced cerebral vasculopathy with abnormal netlike vessels and transdural anastomoses (moyamoya syndrome) is presented. Radiological findings in an additional 40 cases reported in the literature are analyzed, and their clinical relevance is discussed.

Case Description A 19-year-old woman presented with recurrent ischemic brain lesions after radiation therapy for treatment of a craniopharyngioma during childhood. Cerebral angiography 6 and 12 years after completion of radiation therapy revealed progressive cerebral arterial occlusive disease involving the internal carotid artery on either side of the circle of Willis, with abnormal netlike vessels and transdural anastomoses (moyamoya syndrome).

Conclusions Extensive similarities between irradiation-induced cerebral vasculopathy and primary moyamoya syndrome (Nishimoto's disease) support the notion that both disorders share common pathophysiological mechanisms. The occurrence of moyamoya-like vascular changes may not depend on specific trigger mechanisms but may rather represent a nonspecific response of the developing vascular system to a number of various noxious events.

Key Words: brain tumor • cerebral vasculopathy • moyamoya disease • radiation therapy

	Introduction

Top Abstract Introduction Case Report Review of the Literature Discussion References

 
Based on its characteristic neuroradiological appearance, the syndrome consisting of stenosis or occlusion of large and intermediate cerebral arteries, abnormal netlike vessels (ANV), and transdural anastomoses (TDA) has been termed progressive cerebral arterial occlusive disease or moyamoya syndrome.¹ The pathoanatomic basis for this type of vasculopathy is not well understood. In a number of cases, moyamoya vasculopathy may occur in the absence of any apparent associated neurological disorder (primary moyamoya syndrome or Nishimoto's disease).^{2 3 4 5} However, in a subset of patients vasculopathic changes typically occurring in moyamoya syndrome appear to be secondary to a number of nonspecific underlying cerebral vascular disorders such as arteriosclerosis,⁶ thromboembolic events,⁷ inflammatory disorders of cerebral arteries,⁸ spastic disorders,⁷ or, as demonstrated in this report, a complication after radiation therapy.

Progressive cerebrovascular changes after irradiation for treatment of intracranial tumors represent a potentially severe iatrogenic disorder that in a number of patients may significantly reduce the therapeutic value of radiation therapy. This report describes the time course and clinical and radiological findings of typical progressive moyamoya-like vascular changes several years after radiation therapy in a young woman. In addition, the clinical and neuroradiological features of 40 cases of irradiation-induced cerebral vasculopathy reported in the literature are summarized.

	Case Report

Top Abstract Introduction Case Report Review of the Literature Discussion References

 
A 19-year-old woman presented with recurrent sensorimotor transient ischemic attacks in the right half of her body. At the age of 7 a cystic tumor in the region of the sella was diagnosed as craniopharyngioma. She underwent surgery twice in which the tumor was partially removed. After the second operation the patient suffered from panhypopituitarism and subsequently received hormonal substitution therapy. Four months after the second operation the patient had to undergo surgery again because of a large cystic recurrence of the craniopharyngioma. After this operation the patient received cranial irradiation with opposed beams of ⁶⁰Co. The portal field size was 7.5x7.5 cm for each field. The total dose of the irradiation was 50 Gy, with single fractions varying between 0.5 Gy and 2.0 Gy. For the next 5 years the patient's physical and intellectual development was unremarkable. At the age of 13 the patient began to experience psychological and intellectual problems, with rapidly progressing deterioration of her memory and loss of concentration, leading to a failure in her performance at school. One year later, recurrent sensorimotor transient ischemic attacks occurred that initially only involved the left cerebral hemisphere. At that time computed tomography of the brain showed an infarction of the left lentiform nucleus. The basal ganglia showed gross calcifications in both hemispheres. A tumor recurrence was not observed. On carotid angiography a severe stenosis of the left carotid artery with an interhemispheric steal phenomenon and extensive formation of collateral arteries from the external carotid artery could be observed. For the next 5 years the condition of the patient remained stable. At the age of 19 the patient was admitted to our hospital with a severe left hemiparesis, residuals of a right-sided supranuclear facial palsy, and slightly dysarthric speech. Computed tomography revealed a recent additional 2x2-cm ischemic lesion within the right centrum semiovale. Cerebral angiography at this time showed typical and extensive moyamoya-like findings (Figs 1 through 3).

View larger version (155K): [in this window] [in a new window]   Figure 1. Carotid arteriogram of irradiation-induced cerebral vasculopathy. Arteriogram of the right internal carotid artery (sagittal plane) reveals occlusion of the internal carotid artery distal to the branching of the ophthalmic artery. Abnormal netlike vessels are present at the base of the brain and fronto-orbitally. Arrows indicate an unusual anastomosis linking cerebral arteries and the right tentorial artery.

View larger version (138K): [in this window] [in a new window]   Figure 2. Arteriogram of the right external carotid artery (sagittal plane). Transdural anastomoses link the middle cerebral artery (filled arrows) and the meningeal artery on the right (open arrow).

View larger version (126K): [in this window] [in a new window]   Figure 3. Arteriogram of the left external carotid artery (sagittal plane). An occipital transdural net (open arrow) fed by the left external occipital artery provides additional blood supply to the left middle cerebral artery (filled arrows).

The internal carotid arteries exhibited severe changes distal to the ophthalmic artery, with an occlusion on the right and a severe stenosis on the left. Proximal segments of the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA) displayed severe stenosis or were occluded. The blood supply of both hemispheres was provided by an extensive network of collaterals consisting of (1) TDA linking the middle meningeal artery on the right and the right MCA; (2) TDA between the meningeal artery on the left, branches of the left external occipital artery, and the left MCA; and (3) a transdural rete mirabile on the right frontal basis serving as blood supply for the ACA on either side that was fed by the right falx artery and an atypical branch of the tentorial artery. In addition, arteriography revealed basal ANV within the basal ganglia on the left and numerous leptomeningeal anastomoses fed by the PCA on either side.

	Review of the Literature

Top Abstract Introduction Case Report Review of the Literature Discussion References

 
Epidemiology
To date, 40 cases of irradiation-induced occlusive cerebral vasculopathy have been reported in the literature (Table 1). Estimations of the prevalence of the condition are not yet available because of the small number of reports. Progressive irradiation-induced cerebral vasculopathy has been associated with radiation treatment of a variety of intracranial tumors (Tables 1 and 2). Most frequently, the underlying tumor is localized near the sella. In particular, radiation therapy of optic gliomas (34% of cases) appears to predispose patients to the development of progressive cerebral vasculopathy.

View this table: [in this window] [in a new window]   Table 1. Cases of Occlusive Cerebral Vasculopathy After Radiation Therapy

View this table: [in this window] [in a new window]   Table 2. Irradiation-Induced Cerebral Vasculopathy: Underlying Tumor Disorders (n=41)

Although irradiation-induced cerebral vasculopathy occurs in adults and even in elderly patients, the vast majority of patients experience the first symptoms of cerebrovascular disease during childhood: 77% of patients are younger than 18 years, 49% are younger than 4 years, and 18% are younger than 1 year at the time irradiation treatment was performed (Fig 4A).

View larger version (9K): [in this window] [in a new window]   Figure 4. Bar graphs show age distribution at time of radiation therapy in 41 cases of irradiation-induced cerebral vasculopathy (A) and time interval between radiation therapy and occurrence of first clinical symptoms (n=41) (B).

In 85% of cases, the first symptoms of cerebrovascular disease appeared within 8 years after radiation treatment (Fig 4B). The dosage or the type of radiation regimen does not appear to be critical for the development of secondary vascular changes. Cerebral vasculopathy has been observed after doses ranging from 10 to 105 Gy (mean, 52±17 Gy). Several types of radiation procedures have been associated with irradiation-induced cerebrovascular changes. However, the potential relation between radiation strategies used and progressive cerebrovascular changes cannot be stated, since in most reports detailed descriptions of irradiation techniques, field size, fractionation, and total dose are lacking.

Angiographic Findings
Carotid arteriograms reveal severe segmental stenosis or occlusion of cerebral vessels. Most frequently, terminal parts of one or both carotid arteries or its branches, eg, the MCA, are involved (Fig 5). In contrast, stenosis or occlusion of the PCA has been observed in only 4 of 41 patients (References 7, 15, and 20 and the present study). In one patient angiography displayed severe stenosis of the basilar artery.¹⁰

View larger version (20K): [in this window] [in a new window]   Figure 5. Diagram shows site of segmental stenosis or arterial occlusion in irradiation-induced cerebral vasculopathy and frequency of abnormal netlike vessels and transdural anastomoses based on the analysis of 41 cases. ACA indicates anterior cerebral artery; MCA, middle cerebral artery; ICA, internal carotid artery; PCA, posterior cerebral artery; and BA, basilar artery.

Along with segmental stenosis or occlusion of parts of the carotid artery, angiography frequently demonstrates an extensive basal cerebral rete mirabile (ANV) at the base of the brain around and distal to the circle of Willis (Fig 5). In addition, in some patients there is an extensive network of TDA linking meningeal and cerebral arteries. Irradiation during childhood or adolescence appears to predispose patients to the occurrence of ANV and TDA. Whereas in adults only 33% of patients suffering irradiation-induced vasculopathy present with ANV or TDA, ANVs develop in 83% and TDAs in 62% of children or adolescent patients.

Clinical Presentation
In the majority of patients, the symptoms leading to medical examination (focal neurological deficits such as acute hemiparesis) are due to focal ischemic lesions. Other less frequent symptoms include headache, disordered consciousness, vertigo, speech disturbance, or seizures (Table 3). Although impaired mental development is not very frequent at outset (15%), it may become very prominent in the course of the disease (29%). Rarely, pure sensory impairment or involuntary movements are reported.

View this table: [in this window] [in a new window]   Table 3. Irradiation-Induced Cerebral Vasculopathy: Initial Clinical Symptoms

Symptoms in some patients are reported to be transitory; however, in most patients symptoms stabilize and tend to persist. Eight patients (20% of cases) improved in the course of the disease, three of whom received extracranial-intracranial bypass surgery for treatment of cerebrovascular insufficiency. The presence of ANV (and less so TDA) appears to influence the clinical outcome. Patients in whom ANV or TDA was present were more likely to stay clinically stable or to improve, whereas patients in whom ANV or TDA was not present were more likely to deteriorate (Fig 6).

View larger version (23K): [in this window] [in a new window]   Figure 6. Bar graphs show relation between presence of abnormal netlike vessels (left) and transdural anastomoses (right) and clinical outcome. Clinical findings in the course of the disease are categorized as improvement of or stable clinical symptoms or deterioration of symptoms, including death due to cerebral vasculopathic changes.

In four patients sudden death has been ascribed to direct or indirect sequelae of vasculopathic changes. Three of these patients were adults at the time of radiation treatment. In two of these patients TDA or ANV was not present.

	Discussion

Top Abstract Introduction Case Report Review of the Literature Discussion References

 
Progressive cerebral vasculopathy associated with the occurrence of intracranial tumors is rare. Based on the underlying pathophysiological mechanisms, Mori et al¹⁷ differentiated four different types of relations between intracranial tumors and cerebral vasculopathy: (1) induction of vasculopathic changes due to compression of main cerebral arteries by intracranial tumors, (2) cerebral vasculopathy after cranial radiation therapy, (3) cerebrovascular changes and intracranial tumors in the course of neurocutaneous disorders,¹¹ and (4) accidental coincidence of intracranial tumors and primary cerebral vasculopathy.

In our patient occlusive cerebral vasculopathy developed 6 years after radiation therapy. Based on radiological criteria with segmental stenosis of terminal parts and branches of the carotid arteries on both sides, presence of basal ANV, and abnormal TDA, the condition can be diagnosed as secondary moyamoya syndrome. Because angiography as well as computed tomographic and magnetic resonance imaging scans did not reveal any signs of vascular compression by tumor recurrence, nor were there any clinical signs of a neurocutaneous syndrome, it is most likely that the observed vasculopathy represents a long-term complication of radiation therapy for treatment of a craniopharyngioma.

Several lines of evidence suggest that primary moyamoya syndrome and progressive cerebral vasculopathy, such as irradiation-induced cerebral vasculopathy, to a large extent share common pathophysiological mechanisms. Based on radiological criteria, irradiation-induced vascular changes are virtually indistinguishable from primary moyamoya syndrome.^{4 5} In the advanced stages of primary moyamoya syndrome, involvement of the PCA is more common than in irradiation-induced cerebral vasculopathy.³² This finding most likely reflects the fact that in most patients with irradiation-induced cerebral vasculopathy, radiation was targeting areas in the vicinity of the terminal carotid artery or its main branches and hence led primarily to vascular changes in these vessels. Radiation treatment of optic gliomas with portals typically including the carotid siphon may therefore be particularly hazardous.

The presence of ANV and TDA is a typical finding in the third stage of primary moyamoya syndrome^{4 33} and is as frequent in irradiation-induced cerebral vasculopathy. The fact that ANV and TDA are much more frequent in younger patients suggests that the developing vascular system in particular is capable of adapting to severe changes in cerebral blood supply. On the other hand, based on our analysis it is likely that similar to primary moyamoya syndrome, the developing vascular system is more vulnerable to exogenous noxious influences such as irradiation, because the vast majority of patients with irradiation-induced cerebral vasculopathy received radiation during their childhood or adolescence. In irradiation-induced cerebral vasculopathy, the presence of ANV and TDA was associated with a favorable outcome. This finding suggests that the presence and the functional significance of the newly formed abnormal vessels may have some predictive value.

The underlying cause of primary moyamoya syndrome is not yet known. According to pathoanatomic studies, vascular changes primarily involve fibrous thickening of the intima of intermediate and large cerebral arteries in the absence of inflammatory cells or atheroma.³⁴ The adventitia, media, and internal elastic lamina of the affected arteries were normal. Histological data are provided in only three of the cases of irradiation-induced cerebral vasculopathy reviewed here. In those cases, the histological findings resemble those observed in primary moyamoya disease. The most prominent features are fibrous thickening of the intima with marked endothelial proliferation⁹ or collections of foam cells in the intima and extensive myointimal proliferation in the absence of inflammatory vasculitis.²⁰

Although pathoanatomic data on irradiation-induced cerebral vasculopathy are scarce, the striking similarities of primary moyamoya disease and irradiation-induced cerebral vasculopathy support the notion that characteristic clinical and radiological findings in both disorders reflect a nonspecific cascade of pathophysiological events that may be triggered by a variety of underlying conditions. The time course and phenotypic appearance of the underlying process appear to be determined by the vulnerability of the developing cerebral vascular system and its reorganizational capabilities.

Received July 21, 1994; revision received September 9, 1994; accepted September 23, 1994.

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Top Abstract Introduction Case Report Review of the Literature Discussion References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bitzer, M. Articles by Topka, H. Search for Related Content PubMed PubMed Citation Articles by Bitzer, M. Articles by Topka, H.