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(Stroke. 1995;26:1945-1949.)
© 1995 American Heart Association, Inc.

Articles

Spontaneous Thrombosis of an Unruptured Anterior Communicating Artery Aneurysm

An Unusual Cause of Ischemic Stroke

Richard D. Brownlee, MD; Bruce I. Tranmer, MD; Robert J. Sevick, MD; Grigory Karmy, MD Bernadette J. Curry, MD

From the Departments of Clinical Neurosciences (R.D.B., B.I.T., R.J.S., G.K., B.J.C.), Radiology (R.J.S.), Pathology (G.K., B.J.C.), and the Division of Neurosurgery (R.D.B., B.I.T.), University of Calgary, Foothills Hospital, Calgary, Alberta, Canada.

Correspondence to Richard D. Brownlee, MD, Division of Neurosurgery, 1206-3031 Hospital Drive NW, Calgary, Alberta, Canada T2N 4T8.

	Abstract

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Background Stroke caused by spontaneous thrombosis of an unruptured intracranial aneurysm is a rare event.

Case Description A 66-year-old woman experienced a transient ischemic attack and cerebral infarctions due to spontaneous thrombosis of an unruptured anterior communicating artery aneurysm. Extension of thrombus into both anterior cerebral arteries and the left middle cerebral artery, resulting in ischemic infarction in all three vascular territories, was diagnosed by CT scanning, MRI, and cerebral angiography and confirmed at autopsy.

Conclusions This case illustrates a rare complication of an unruptured saccular aneurysm with neuroimaging and pathological correlation. Morphological and hemodynamic factors that may have precipitated aneurysm thrombosis are discussed with reference to experimental models.

Key Words: aneurysm • cerebral ischemia, transient • pathology • thrombosis

	Introduction

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Cerebral aneurysms carry a high risk of morbidity and mortality. This most commonly results from subarachnoid hemorrhage due to aneurysm rupture. We present a rare case of transient ischemic attack (TIA) and ischemic stroke resulting in death due to spontaneous thrombosis of an unruptured anterior communicating artery aneurysm.

Review of the literature suggests that complete thrombosis of intracranial aneurysms is uncommon. It most frequently occurs after subarachnoid hemorrhage and in fusiform or giant saccular aneurysms. In autopsy series thrombosis of intracranial aneurysms has been found in 9% to 13% of cases.^{1 2 3 4} Aneurysm thrombosis after subarachnoid hemorrhage^{3 4 5 6 7 8 9 10} has a reported incidence of 1% to 2%.^{4 5} This may be as high as 3% in patients treated with antifibrinolytic agents⁴ or may be a delayed event after subarachnoid hemorrhage.³ Spontaneous thrombosis of giant intracranial aneurysms^{11 12 13 14 15 16 17} may be evident in up to 55% of lesions demonstrated on CT scans.¹¹ Thrombosis is usually partial, with complete thrombosis occurring in 13% to 20% of cases.^{18 19 20} Parent or distal artery occlusion has been reported in association with aneurysm thrombosis after subarachnoid hemorrhage,^{13 14} during treatment with antifibrinolytic agents,^{4 21} after endovascular treatment,²² and in patients with unruptured giant cerebral aneurysms.^{14 15 16 17 19} Unruptured, partially thrombosed aneurysms may serve as a source of emboli leading to TIAs^{11 23 24 25} or cerebral infarction.^{13 14 15 26 27}

We present a case in which a TIA was followed by strokes that progressively involved several vascular territories due to thrombosis of a large, unruptured anterior communicating artery aneurysm. This rare complication of a cerebral aneurysm is supported by neuroimaging and pathological correlation. Pathogenetic mechanisms for aneurysm thrombosis are discussed with reference to experimental models.

	Case Report

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A 66-year-old female patient was admitted to a local hospital with acute onset of left hemiparesis. Approximately 2 weeks before admission the patient experienced a presyncopal episode with bilateral leg weakness that was transient and resolved spontaneously. The patient did not seek medical attention at that time.

On the day of admission the patient awoke in normal health. Shortly thereafter she developed an acute left hemiparesis and inability to walk. She experienced no headache and no alteration in her level of consciousness. At the time of admission, the patient was alert and oriented, appeared dehydrated, and had a left hemiparesis. The remainder of her neurological and general physical examination was normal. Laboratory investigations revealed a creatinine level of 160 µmol/L and a mild metabolic acidosis associated with her documented history of chronic renal failure. The white blood cell count was mildly elevated at 12.0x10⁹/L, and her coagulation profile was abnormal with an elevated partial thromboplastin time of 37.1 seconds (control, 29.0 seconds) and international normalized ratio of 1.59.

During the 48 hours after admission the patient exhibited a progressive deterioration in her level of consciousness. She became drowsy, opened her eyes to voice, occasionally verbalized to painful stimulation, and withdrew only her right arm and leg to pain. A head CT scan (Fig 1) revealed a hyperdense lesion in the region of the anterior communicating artery and cerebral infarction in the right anterior cerebral artery (ACA) territory but no evidence of subarachnoid hemorrhage. The patient was transferred for neurosurgical consultation.

View larger version (107K): [in this window] [in a new window]   Figure 1. A, Nonenhanced axial CT scan demonstrating an extra-axial hyperdense lesion in the midline, just above the suprasellar cistern. Minimal surrounding hypodensity is seen in the right frontal lobe as a result of edema. B, Nonenhanced axial CT cut obtained at a level cephalad to A shows hypodensity involving cortex and subcortical white matter of the medial aspects of the frontal and parietal lobes on the right. Appearance is consistent with right anterior cerebral artery territory infarction.

An MR scan was performed on the day of transfer (Fig 2) and revealed a thrombosed anterior communicating artery aneurysm, absent signal void in the right ACA, and areas of cortical ischemia in the right ACA territory. A cerebral angiogram performed the following day (Fig 3) showed occlusion of both ACAs and no opacification of the thrombosed aneurysm. The patient's condition deteriorated, and a repeated CT scan performed on the fifth day after admission (Fig 4) showed evidence of infarction in both ACAs and the left middle cerebral artery territories. In view of her poor clinical status and extensive cerebral infarcts, aggressive care was discontinued. The patient died 7 days after admission to the hospital.

View larger version (109K): [in this window] [in a new window]   Figure 2. A, Coronal T1-weighted MR scan (repetition time, 500 milliseconds; echo time, 19 milliseconds) shows an extra-axial, isointense lesion in the midline subfrontal area (arrows), measuring approximately 15 mm in diameter. B, Axial T2-weighted image (repetition time, 3200 milliseconds; echo time, 90 milliseconds) demonstrates marked signal hypointensity within the lesion. Signal intensities indicate the presence of acute thrombus (deoxyhemoglobin). Surrounding signal hyperintensity represents edema. Other images (not shown) showed absent flow-related signal void in the distal right anterior cerebral artery.

View larger version (119K): [in this window] [in a new window]   Figure 3. Left, Anteroposterior (AP) view, digital subtraction arteriogram, right common carotid (RCC) artery injection. The A1 segment of the right anterior cerebral artery is occluded. There is no filling of the anterior communicating artery aneurysm or distal anterior cerebral artery segments. Right, AP view of the left common carotid (LCC) artery injection shows occlusion of a small A1 segment (arrows).

View larger version (110K): [in this window] [in a new window]   Figure 4. Nonenhanced axial CT scan shows areas of hypodensity bilaterally in the anterior cerebral artery territories as well as in the left middle cerebral artery territory, consistent with multifocal infarction.

Autopsy Findings
Gross examination of the brain in the fresh state revealed an intact 2.3x1.3-cm-diameter anterior communicating artery aneurysm (Fig 5) with no evidence of recent or remote subarachnoid hemorrhage. Thrombus filled the aneurysm (Fig 6), the right A1, and both A2 segments of the ACAs. The left A1 segment was hypoplastic and contained no clot. Cortical infarcts were evident in the territories of both ACAs and the left middle cerebral artery.

View larger version (0K): [in this window] [in a new window]   Figure 5. Gross photograph showing the thrombosed anterior communicating artery aneurysm at the base of the brain. The optic nerves and chiasm have been retracted to expose the anterior cerebral and anterior communicating arteries in relation to the aneurysm.

View larger version (74K): [in this window] [in a new window]   Figure 6. Gross photograph of the aneurysm and associated arteries. The aneurysm has been cut in half, revealing thrombus within its lumen. The aneurysm arose from the anterior communicating artery close to the dominant A1 segment of the right anterior cerebral artery.

Histological examination of the aneurysm after fixation revealed a dome with an internal diameter of 17x11 mm, which was filled with recent thrombus (Fig 7). The orifice of the aneurysm was 1.5 mm in diameter, and the dome of the aneurysm arose from the parent vessel with a neck 1.6 mm long (Fig 8). The dome of the aneurysm exhibited the characteristic absence of an elastic lamina and deficiency of the tunica media²⁸ with no atherosclerotic changes or calcification. No site of aneurysm rupture was identified, and there was no evidence of iron pigment in the leptomeninges or on the external surface of the aneurysm. The right A1 segment and both A2 segments of the ACA were also filled with recent thrombus. Microscopic examination of the cortical infarcts showed emboli within small subarachnoid arteries adjacent to large areas of dead eosinophilic neurons.

View larger version (0K): [in this window] [in a new window]   Figure 7. Photograph of the microscopic appearance of the aneurysm with a Movat stain for elastin. The dome of the aneurysm has a thin wall devoid of elastic lamina or muscular media. Recent thrombus in various stages of organization fills the dome of the aneurysm. The thrombosed A2 segment of the right anterior cerebral artery can be seen adherent to the dome of the aneurysm.

View larger version (0K): [in this window] [in a new window]   Figure 8. Photograph of the microscopic appearance of the aneurysm at its site of origin from the parent artery. The Movat stain accentuates the elastic lamina in the parent artery and neck of the aneurysm. The small orifice (1.5 mm) and short neck (1.65 mm) of the aneurysm are easily identified. Recent thrombus fills the aneurysm dome and neck as well as the anterior communicating artery.

The general autopsy revealed evidence of emphysema, chronic pancreatitis, and chronic renal failure. A right lower lobe pneumonia with abscess formation was identified and believed to be the ultimate cause of death. An incidental mucinous adenocarcinoma of the pancreas was also identified. Examination of the heart and carotid arteries revealed no source of cerebral emboli, and no embolic infarcts were identified elsewhere in the body.

	Discussion

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While rupture is a common complication of intracranial aneurysms, spontaneous thrombosis of unruptured aneurysms is uncommon, and its pathogenic mechanisms are unknown. Factors associated with aneurysm thrombosis after subarachnoid hemorrhage may include hypotension, vasospasm, and local damage to the arterial wall.^{2 3 9} In our patient there was no history or evidence of subarachnoid hemorrhage, and no hypotensive episodes were observed. Thrombosis of unruptured aneurysms has been associated with calcification within the atherosclerotic wall of giant saccular^{1 10 11} and fusiform²⁷ aneurysms. The aneurysm in this case revealed typical microscopic features of a saccular aneurysm with loss of elastic lamina and degeneration of the muscular media²⁸ but no evidence of atherosclerosis or calcification.

The aneurysm in our patient measured 2.3x1.3 cm in the fresh postmortem state. Although thrombus filled the lumen and may have limited shrinkage artifact, the aneurysm still could have been larger than 2.5 cm in vivo and would therefore be classified as a giant aneurysm. Since most previous reports of aneurysm thrombosis also involved large to giant-sized aneurysms,^{11 12 13 14 15 16 17 18 19 20 24 25} size may be an important factor in precipitating thrombosis of unruptured aneurysms. In an experimental animal model of aneurysms, Black and German²⁹ suggested that a ratio of chamber volume (in cubic millimeters) to orifice area (in square millimeters) of greater than 28:1 was associated with aneurysm thrombosis. In our patient we found a chamber volume of 1615.56 mm³ and an orifice area of 1.77 mm² for a ratio of 912.75, which is well above the ratio associated with aneurysm thrombosis. In a different model, Roach³⁰ suggested that aneurysms with a length (height) greater than 4 times the tube diameter at the orifice thrombosed, while those 2 to 2.5 times the tube diameter ruptured. The aneurysm in our patient had an elliptical shape 17 mm long and 11 mm wide (internal dimensions), with an orifice diameter of 1.5 mm. The length was therefore 11 times the tube diameter at the orifice and would be predicted to thrombose. An autopsy series suggested that aneurysms may be 30% to 60% smaller postmortem than in their in vivo state.³¹ Although this may have confounded our comparison with the experimental models, the presence of thrombus within the aneurysm and associated vessels may have minimized shrinkage. In addition, the aneurysm dome and neck should have experienced a similar degree of shrinkage. Therefore, we believe that the experimental models can be extrapolated to the aneurysm in our patient.

Experimental models have also shown that flow in large aneurysms is complicated by blood stagnation, increased blood viscosity, and slow flow that may lead to aneurysm thrombosis,³² which has been reported in large or giant saccular aneurysms.^{11 12 13 14 15 16 17 18 19 20 24 25} Aneurysms with a small orifice experience lower flow velocity, different flow direction, and smaller shear forces than those with a large orifice.³² In our patient the aneurysm dome was large (ID, 17x11 mm) and the orifice was small (1.45 mm), both of which could produce a low-flow state and promote thrombosis. Platelet deposition in giant aneurysms³³ and turbulent blood flow in saccular aneurysms²⁸ have been demonstrated in humans. Endothelial injury due to turbulent blood flow facilitates platelet deposition, platelet aggregation, and thrombus formation.^{33 34} Therefore, a number of factors probably interacted to cause thrombosis of the large, unruptured aneurysm in our patient.

Location may also be important as a risk factor for TIAs or stroke from thrombosed saccular aneurysms. The most commonly reported sites are the ICA^{11 13 14 15 23} and middle cerebral artery.^{14 23 24} Thrombosis of fusiform aneurysms of the basilar,²⁷ posterior cerebral,²⁶ and cavernous carotid¹⁴ arteries has also been reported to cause TIAs or strokes. Similar events from an unruptured anterior communicating artery aneurysm, as in our patient, have not previously been reported.

Medical factors that may have contributed to aneurysm thrombosis in our patient include the presence of an occult malignancy³⁵ and dehydration. These factors could have induced a setting of decreased blood flow and increased coagulability,³⁵ which may have precipitated aneurysm thrombosis and extension of thrombus into adjacent vessels, resulting in ischemic stroke. Thrombosis of the aneurysm occurred despite an elevated partial thromboplastin time and international normalized ratio, which was thought to be related to alcoholic liver disease. At autopsy hepatic steatosis but no sclerosis was identified.

Although both TIAs and strokes may result from thrombosis of unruptured intracranial aneurysms, our patient is unusual in the progression of her symptoms from a single TIA to cerebral infarctions involving several vascular territories. Stroke resulting from spontaneous thrombosis of unruptured intracranial aneurysms is rare, occurring most often in giant^{11 13 14 15} and fusiform^{26 27} aneurysms. In our patient with thrombosis of a large, unruptured anterior communicating artery aneurysm, CT and MRI suggested the diagnosis, which was confirmed at autopsy. Cerebral angiography demonstrated occlusion of adjacent vessels, which was due to thrombus extending from the aneurysm into the dominant right A1 and both A2 segments of the ACA. The hypoplastic left A1 contained no clot at autopsy, possibly as a result of lysis or embolization. Pathological examination of the brain revealed emboli within small subarachnoid arteries adjacent to large cortical infarcts in the vascular distribution of both ACAs and the left middle cerebral artery.

The presyncopal episode associated with transient bilateral leg weakness that our patient experienced 2 weeks before admission probably represented an embolic TIA arising from her thrombosed aneurysm. TIAs resulting from partially thrombosed intracranial aneurysms are uncommon,^{14 23 24 25} although thromboembolism from clot-containing intracranial aneurysms has been reported to occur in 5% to 59% of cases.^{11 33} Therefore, patients with TIAs in whom no other source of emboli can be identified should be investigated with cerebral angiography,²³ CT, or MRI to identify a thrombosed aneurysm as a potential source of emboli.

The optimal form of treatment for patients with a thrombosed cerebral aneurysm has not been well defined. TIAs resulting from these lesions have been treated medically with antiplatelet agents²³ and surgically by aneurysm clipping^{14 23 24} with no apparent difference in outcome.²³ However, it has been reported that intra-aneurysmal clot does not protect against aneurysm rupture¹¹ and that TIAs may precede subarachnoid hemorrhage.^{23 36} Therefore, surgical treatment of thrombosed aneurysms may be the preferred treatment since it has been shown to alleviate TIAs^{14 23 24} and would reduce the risk of subarachnoid hemorrhage.

In summary, this case represents a rare but important complication of intracranial aneurysms. Imaging and pathological correlation provide further evidence that unruptured saccular aneurysms may thrombose and give rise to TIAs and stroke. The pathophysiology of aneurysm thrombosis is discussed in relation to animal models, although the exact cause in our patient could not be identified.

Received February 20, 1995; revision received May 3, 1995; accepted May 31, 1995.

	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 Brownlee, R. D. Articles by Curry, B. J. Search for Related Content PubMed PubMed Citation Articles by Brownlee, R. D. Articles by Curry, B. J.