(Stroke. 2001;32:817-a.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
Cerebral Infarction Throughout Both Internal Carotid Arteries Detected by Diffusion-Weighted MRI
Third Department of Internal Medicine, Shimane Medical University, Shimane, Japan
To the Editor:
Many recent reports have shown that diffusion-weighted MRI (DWI) is a sensitive method for detecting the early changes of cerebral infarction. Bilateral internal carotid artery (ICA) occlusion infrequently has an acute onset and rarely causes cerebral infarction throughout the territories of both ICAs. We report one such case, in which cerebral infarction was detected by DWI.
An 85-year-old man who had suddenly become comatose was
admitted to our hospital. He had a history of right cerebellar embolism
in the posterior inferior cerebellar artery caused by
chronic atrial fibrillation 2 years earlier. He was being treated with
warfarin in another hospital and had remained symptom free for 2 years
until this admission. Physical examination on admission revealed a
deeply comatose patient (Glasgow Coma Scale score of 3) with
Cheyne-Stokes respiration. His blood pressure was 210/130 mm Hg
and pulse was 130 bpm with irregular rhythm. There were no neck bruits.
Radial and femoral pulses were palpable in both sides. Lung and heart
auscultation were normal. Neurological examination revealed roving eye
movements with reactive pupils of unequal size (right pupil 2.5
mm, left pupil 3.5 mm), a normal oculocephalic reflex, and
decerebrate rigidity on pain stimulation. There was moderately
increased tone in the extremities and no pathological reflexes.
Laboratory investigations revealed normal values for electrolytes,
blood cell count, renal and liver function, blood glucose and lipid
levels, coagulation studies, and erythrocyte sedimentation rate. A
serological test for syphilis was negative. An ECG showed atrial
fibrillation and left ventricular hypertrophy.
The chest x-ray showed slight cardiomegaly. Transthoracic
echocardiograms showed a small thrombus in the left atrium. A duplex
scan revealed no stenosis in the carotid bulbs or proximal
ICAs. The patient was intubated. Three hours after onset, emergency T1-
and T2-weighted MRI findings were normal except for an old cerebellar
infarction in the right posterior inferior cerebellar
artery and did not show transtentorial herniation. DWI showed diffuse
hyperintensities involving both hemispheres in the territory of the
ICAs
(Figure 1
), and the territory of the posterior cerebral
artery and brain stem was spared. There was no flow in either ICA on MR
angiography
(Figure 2). Urokinase (420 000 IU) and osmotic
diuretics were administered by intravenous
infusion, but these were ineffective, and the patient died 26 hours
after admission. His family refused permission for an
autopsy.
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Bilateral ICA occlusion is known to cause fatal stroke.1 However, the clinical course of such patients is often chronic,1 due to collateral circulation, and most strokes result from severe atherosclerosis,1 arteritis2 and similar processes. There have been few reports of acute cerebral infarction throughout both ICAs with spontaneous and simultaneous bilateral carotid artery occlusion. To our knowledge, only 2 such cases have been reported previously, excluding trauma or iatrogenic cases. Browne et al3 reported a case in which an atrial myxoma caused fatal multiple organ embolization that included both ICAs and the cerebellum, heart, kidney, and spleen. Yamaguchi et al4 reported a case of simultaneous bilateral carotid occlusion. Although they did not observe cerebral infarction on CT scan or MRI, angiography revealed bilateral occlusion of the ICAs. Although postmortem examination did not reveal myxoma, the bilateral ICA was occluded by fresh thrombi at the carotid bifurcation in their case, and they suspected cardiogenic embolism from the clinical course and autopsy findings. It is an undeniable possibility that the cerebral infarction in our patient was caused by dissection of the carotid arteries, either simultaneous and bilateral, or of 1 carotid artery, with the other previously occluded. However, because of the sudden onset stroke attack, history of atrial fibrillation, and the small intra-atrial thrombosis detected by the transthoracic echocardiogram, we speculate that the infarction was also caused by a cardiogenic embolism. In our case, an embolus from the heart likely occluded both ICAs simultaneously and produced cerebral infarction throughout both ICAs. Alternatively, our patient might have had asymptomatic unilateral ICA occlusion with collateral circulation through the anterior communicating arteries from the normal ICA, which was then occluded by a cardiac embolus. There is no convincing evidence, because an autopsy was not performed.
Lövblad et al5 described a comatose patient whose DWI findings showed diffuse hyperintensities involving both hemispheres; transtentorial herniation with compression of the brain stem and an absence of flow in the carotid arteries was also noted, but the lesions on DWI extended to almost whole brain. They concluded that the lesions and absence of flow in the carotid arteries had resulted from brain death. However, we speculate that the lesions in our case were the result of acute ischemic change caused by sudden bilateral ICA occlusion, because the DWI lesion corresponded completely to the territory of bilateral ICA. To our knowledge, MR findings that show cerebral infarction throughout both ICAs have not been reported previously. In this case, we could not detect stroke lesions by conventional MRI (T1- and T2-weighted, FLAIR), because we performed MRI soon after the onset of the stroke. DWI is a sensitive method for detecting the early changes of cerebral infarction. This case may be the first report of a case of cerebral infarction in both ICAs detected by DWI.
References
1. Groch SN, Hurwitz LJ, McDonnel F. Bilateral carotid artery occlusive disease: a report of four patients. Arch Neurol. 1960;2:130–133.
2. Howard GF, Ho SU, Kim KS, Wallach J. Bilateral carotid artery occlusion resulting from giant cell arteritis. Ann Neurol. 1984;15:204–207.[Medline] [Order article via Infotrieve]
3.
Browne WT,
Wijdicks EF, Parisi JE, Viggiano RW. Fulminant brain necrosis from
atrial myxoma showers. Stroke. 1993;24:1090–1092.
4. Yamaguchi S, Oki S, Ogasawara H, Sato H, Ito Y, Hibino S. A case of simultaneous bilateral carotid occlusion. No Shinkei Geka. 1997;25:247–251.[Medline] [Order article via Infotrieve]
5.
Lövblad KO,
Basssetti C. Diffusion-weighted magnetic resonance imaging in brain
death. Stroke. 2000;31:539–542.
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