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PubMed2001

[Brain infarction related to hepatic arterial infusion chemotherapy].

We examined the occurrence of brain infarction with hepatic arterial infusion chemotherapy for liver cancer. One hundred and eighty-one cases of hepatic arterial infusion chemotherapy were carried out for liver cancer patients in 4 hospitals associated with Osaka University 2nd Dept. of Surgery. These included metastatic (n = 103) and primary (n = 78) liver tumors. The medication was mainly 5-FU with/without CDDP and IFN. Catheters were inserted via the left subclavian artery in 106 cases and via the femoral artery in 75 cases. Among these patients, brain infarctions occurred in seven patients. Occlusions were found in the cerebellum (n = 3), thalamus (n = 1), brain stem (n = 1) and TIA (n = 2). All these patients had catheterization from the left subclavian artery. Furthermore, 64 patients of Ikeda Municipal Hospital were examined and analyzed for brain infarction, in order to eliminate the difference between facilities (all patients in Ikeda Municipal Hospital were catheterized via the left subclavian artery). Many more brain infarctions occurred in metastatic liver cancer patients than in primary liver cancer patients. The hemostasis function deteriorated in primary liver cancer patients, and is thought to be involved in the brain infarction. Six of seven cases of brain infarction occurred in vertebral artery supply area. It may be that the occurrence of brain infarction was related to the flow of the blood vessels.

Aged↗
PubMed2002

Homocysteine, silent brain infarcts, and white matter lesions: The Rotterdam Scan Study.

Silent brain infarcts and white matter lesions are frequently seen on magnetic resonance imaging in healthy elderly people and both are associated with an increased risk of stroke and dementia. Plasma total homocysteine may be a potentially modifiable risk factor for stroke and dementia. We examined whether elevated total homocysteine levels are associated with silent brain infarcts and white matter lesions. The Rotterdam Scan Study is a population-based study of 1,077 people aged 60 to 90 years who had cerebral magnetic resonance imaging. The cross-sectional relation of total homocysteine with silent infarcts and white matter lesions was analyzed with adjustment for cardiovascular risk factors. The mean plasma total homocysteine level was 11.5 micromol/l (standard deviation 4.1). The risk of silent brain infarcts increased with increasing total homocysteine levels (odds ratio 1.24/standard deviation increase, 95% confidence interval 1.06-1.45). The severity of periventricular white matter lesions and extent of subcortical white matter lesions were also significantly associated with total homocysteine levels, even after excluding those with silent brain infarcts. The overall risk of having either a silent brain infarct or severe white matter lesions was strongly associated with total homocysteine levels (odds ratio 1.35/standard deviation increase, 95% confidence interval 1.16-1.58). We concluded that total homocysteine levels are associated with silent brain infarcts and white matter lesions independent of each other and of other cardiovascular risk factors.

Aged↗
PubMed2003

Silent brain infarcts and the risk of dementia and cognitive decline.

BACKGROUND: Silent brain infarcts are frequently seen on magnetic resonance imaging (MRI) in healthy elderly people and may be associated with dementia and cognitive decline. METHODS: We studied the association between silent brain infarcts and the risk of dementia and cognitive decline in 1015 participants of the prospective, population-based Rotterdam Scan Study, who were 60 to 90 years of age and free of dementia and stroke at base line. Participants underwent neuropsychological testing and cerebral MRI at base line in 1995 to 1996 and again in 1999 to 2000 and were monitored for dementia throughout the study period. We performed Cox proportional-hazards and multiple linear-regression analyses, adjusted for age, sex, and level of education and for the presence or absence of subcortical atrophy and white-matter lesions. RESULTS: During 3697 person-years of follow-up (mean per person, 3.6 years), dementia developed in 30 of the 1015 participants. The presence of silent brain infarcts at base line more than doubled the risk of dementia (hazard ratio, 2.26; 95 percent confidence interval, 1.09 to 4.70). The presence of silent brain infarcts on the base-line MRI was associated with worse performance on neuropsychological tests and a steeper decline in global cognitive function. Silent thalamic infarcts were associated with a decline in memory performance, and nonthalamic infarcts with a decline in psychomotor speed. When participants with silent brain infarcts at base line were subdivided into those with and those without additional infarcts at follow-up, the decline in cognitive function was restricted to those with additional silent infarcts. CONCLUSIONS: Elderly people with silent brain infarcts have an increased risk of dementia and a steeper decline in cognitive function than those without such lesions.

Aged↗
PubMed2001

Activated astrocytes with glycogen accumulation in ischemic penumbra during the early stage of brain infarction: immunohistochemical and electron microscopic studies.

Brain infarction was induced in rats by injection of microspheres through the right internal carotid artery, and structural changes in the astrocytes were observed during the early period following the infarction. Necrotic foci, varying in size and shape, were found in the right hemisphere. After immunohistochemical staining for GFAP, GFAP-positive astrocytes in the perinecrotic area known as the ischemic penumbra had distinctly increased in number and size with elongation of cytoplasmic processes 3 days after infarction. Electron microscopic observation revealed that glycogen granules had markedly accumulated in the cytoplasm of astrocytes located in the ischemic penumbra 3 and 5 days after infarction. Seven days after infarction, however, the glycogen granules disappeared from the astrocytes. Intermediate filaments increasingly appeared in the protoplasmic astrocytes after 3 days and were abundant in the activated and hypertrophied astrocytes after 7 days. As a result of our present study, we conclude that: (1) the function of glucose uptake from blood vessels was not impaired in the astrocytes under hypoxic conditions; (2) the astrocytes actively ingested blood glucose through the endothelial cells and accumulated it as glycogen for activation of their functions, and the cell volume increased under hypoxic conditions; (3) the depression of energy metabolism and the decrease in the uptake of energy sources in the nerve cells promoted glycogen accumulation in the astrocytes under hypoxic conditions; (4) intermediate filaments (GFAP filaments) increased in number, coincident with the activation and enlargement of the astrocytes; and (5) protoplasmic astrocytes were transformed into fibrous astrocytes in the ischemic penumbra of the brain infarction.

Animals↗
PubMed2000

The relationship between angiotensinogen gene CD235 met-->Thr substitution polymorphism and brain infarction in Chinese.

OBJECTIVE: To detect the relationship between angiotensinogen (AGT) gene CD235 Met-->Thr substitution polymorphism and brain infarction. METHODS: The CD235Met-->Thr substitution polymorphism in exon 2 of AGT gene was analyzed in normal group(82 cases) and brain infarction group (102 cases) by a combination of polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP). RESULTS: Between the control group and brain infarction group, chi-square test showed no significant difference in the frequencies of T/T genotype and T allele (P>0.05). However, the frequencies of T/T genotype and T allele (70.6% and 83.8%) for multiple brain infarction patients were higher than those (42.6% and 65.2%) for lacunae brain infarction patients and those (42.0% and 65.2%) for controls (P<0.01). The frequencies of AGT T/T genotype and T allele (65.3% and 78.6%) for patients with brain infarction associated with hypertension were higher than those (42.0% and 65.0%) for patients with brain infarction not associated with hypertension (P<0.05). CONCLUSION: No direct relationship between AGT CD235 Met-->Thr substitution polymorphism and ordinary brain infarction has been observed, but there is a significant correlation between AGT gene T/T genotype and multiple brain infarction, and brain infarction associated with hypertension too.

Adult↗
PubMed1989

Snoring as a risk factor for sleep-related brain infarction.

We studied 177 consecutive male patients aged 16-60 years with brain infarction verified by neuroradiology and analyzed the time of onset of stroke symptoms related to sleep and the role of possible or known risk factors for brain infarction. Brain infarction occurred relatively more often during the first 30 minutes after awakening than at any other time. In multiple stepwise logistic regression analyses, snoring was the only independent risk factor differentiating stroke occurring during sleep and stroke occurring either during sleep or during the first 30 minutes after awakening from stroke occurring at other times of the day. The risk ratios were 2.65 (95% confidence interval 1.32-5.29, p less than 0.005) and 3.16 (95% confidence interval 1.61-6.22, p less than 0.001), respectively. Other factors tested were age, arterial hypertension, diabetes mellitus, smoking, alcohol consumption, and body mass index. Arterial hypertension seemed to have an additive effect on the independent risk caused by snoring.

Adolescent↗
PubMed1996

Brain infarction caused by syphilitic aortic aneurysm. A case report.

Neurosyphilis often develops brain infarction. Recently, the authors experienced a case of brain infarction caused by syphilitic aneurysm on the thoracic aorta, and its clinical significance is reported. A seventy-eight-year-old woman with strongly positive serologic tests for syphilis suddenly developed global aphasia and right hemiplegia. Brain computed tomography (CT) showed a large brain infarction in the left middle cerebral artery territory. A huge aneurysm of the ascending aorta eroded the sternum and the second and third ribs. The left common carotid artery was completely compressed by the aneurysm, and blood flow was not demonstrated on enhanced CT. A cerebrospinal fluid examination revealed normal cell counts, and the titer of a syphilis test was very low. She did not have any arrhythmia, ischemic heart disease, or valvular heart disease as an embolic source. Brain infarction may be developed by pressure of an aortic aneurysm on the left common carotid artery. They recommend consideration of syphilis as an etiology of brain infarction when luetic patients are seen in old age.

Aged↗
PubMed1994

[Horner type anisocoria associated with brain infarction of the internal carotid artery axis].

Brain infarction caused by arterial occlusion of the internal carotid axis sometimes develops Horner syndrome. The purpose of this study is to clarify the characteristics and mechanism of "Horner type" anisocoria, which is one of the symptoms of Horner syndrome, in patients with brain infarction in regions supplied by the internal carotid artery (ICA). We studied 112 consecutive patients (71 males and 41 females, mean age of 60.8 +/- 12.3 years) with brain infarction with either ICA or the middle cerebral artery (MCA) occlusion, who were admitted to the National Cardiovascular Center within seven days after the onset of stroke. We examined differences in frequency of Horner type anisocoria and its duration after onset by the mechanism (embolic or thrombotic) and site (ICA proximal, ICA distal or MCA) of arterial occlusion. Horner type anisocoria was seen in 26 of 66 cases (39.4%) with embolic occlusion, which was more frequent than in those with thrombotic occlusion (8 of 46 cases, 17.4%) (p < 0.05). In the embolic occlusion group, Horner type anisocoria was seen in 17 of 32 cases (53.1%) with ICA occlusion, which was more frequent than in those with MCA occlusion (9 of 34 cases, 26.5%) (p < 0.05). Horner type anisocoria was more frequently seen in embolic (17 of 32 cases, 53.1%) than in thrombotic ICA occlusion (2 of 21 cases, 9.5%) (p < 0.01). The duration of Horner type anisocoria was shorter in patients with either distal ICA or MCA occlusion than in those with proximal ICA occlusion (p < 0.05). In patients with thrombotic occlusion, there was no distinct characteristics in between those ICA and MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Elevated intracranial pressure following brain infarction--a retrospective study].

Brain infarction is a frequent cause of emergency admission to hospital. We have made a retrospective study in order to describe patients who develop fatally elevated intracranial pressure. From 1991 to 1993, seven patients (3.3%) died within the first 96 hours after the symptoms appeared. All these patients died from elevated intracranial pressure caused by oedema in and around an infarction in the territory of the middle cerebral artery. These patients were significantly younger than the general population of patients with infarction (p < 0.01), and also younger than the patients who died from other causes during the observation period (p < 0.01). We think that these cases underline the importance of establishing effective acute treatment for ischemic cerebrovascular diseases, since this is probably the only effective way to protect against formation of oedema.

Adult↗
PubMed1992

Elevated lactate and alkalosis in chronic human brain infarction observed by 1H and 31P MR spectroscopic imaging.

The goal of this study was to investigate lactate and pH distributions in subacutely and chronically infarcted human brains. Magnetic resonance spectroscopic imaging (MRSI) was used to map spatial distributions of 1H and 31P metabolites in 11 nonhemorrhagic subacute to chronic cerebral infarction patients and 11 controls. All six infarcts containing lactate were alkalotic (pHi = 7.20 +/- 0.04 vs. 7.05 +/- 0.01 contralateral, p less than 0.01). This finding of elevated lactate and alkalosis in chronic infarctions does not support the presence of chronic ischemia; however, it is consistent with the presence of phagocytic cells, gliosis, altered buffering mechanisms, and/or luxury perfusion. Total 1H and 31P metabolites were markedly reduced (about 50% on average) in subacute and chronic brain infarctions (p less than 0.01), and N-acetyl aspartate (NAA) was reduced more (approximately 75%) than other metabolites (p less than 0.01). Because NAA is localized in neurons, selective NAA reduction is consistent with pathological findings of a greater loss of neurons than glial cells in chronic infarctions.

Adult↗
PubMed2005

Transient body fluid accumulation and enhanced NKCC2 expression in gerbils with brain infarction.

BACKGROUND: Enhanced expression of a kidney-specific sodium co-transporter (NKCC2: Na-K-2Cl co-transporter) in the thick ascending limb of Henle has been identified in rat models of congestive heart failure and liver cirrhosis, suggesting that high NKCC2 expression underlies edema formation. An increased abundance of NKCC2, however, has also been noted in rats with the syndrome of inappropriate secretion of antidiuretic hormone; hyponatremia without edema. In the present study, we examined NKCC2 expression in non-edematous disease, such as a brain infarction, and investigated the physiological and/or pathological characterization of NKCC2 expression. METHODS: We initially examined NKCC2 expression in an animal model of brain infarction. Mongolian gerbils (around 60 g body weight) underwent bilateral clamping of the common carotid arteries for 5 min for the induction of brain infarction. NKCC2 and apical water channel (AQP2) protein levels in the collecting duct were examined by Western blotting in kidney tissues 2, 7, and 14 days after the brain infarction. Gerbils with brain infarction were then fed either a normal low-sodium diet (0.3 g/kg/day) or a high-sodium diet (3.0 g/kg/day), and body weight, urine volume and urinary osmolality were examined daily. Blood parameters were measured on day 14 after the brain infarction. RESULTS: Histochemical examination of the brain confirmed the presence of brain infarction, as manifested by altered cresyl violet staining in the hippocampus. Protein levels of NKCC2 were significantly increased in gerbils with brain infarction on days 2 and 7 after brain infarction, whereas AQP2 protein signals remained unaltered. However, the increased NKCC2 intensity disappeared on day 14. Body weight gain was slightly, but significantly greater in gerbils with brain infarction than in sham-operated gerbils up to 7 days after the brain infarction. The high-sodium diet resulted in significant urinary concentration and enhanced weight gain in infarcted gerbils. CONCLUSION: We noted increased NKCC2 abundance in non-edematous disease, which enhanced body fluid accumulation, likely via the sodium loading-dependent concentration of the urine. These results suggest that the physiological process of edema formation is based on specific NKCC2 expression. The transient duration of these findings in the present animal model suggests two different characteristics of specific NKCC2 expression, an immediate, transient appearance as a common response in serious conditions and more chronic expression that leads to edema formation.

Animals↗
PubMed2000

[Acute surgical and endovascular therapy for stroke: especially patients with brain infarction].

From January 1994 to December 1997, 845 patients with stroke were admitted to Hakodate Municipal Hospital. They consisted of 514 patients with brain infarction, 206 with brain hemorrhage, 121 with subarachnoid hemorrhage and 4 with intracranial hemorrhage from arteriovenous malformation. The clinical categories of brain infarction were as follows; atherothrombotic recognized in 158 patients, cardioembolic in 114, lacunar in 217 and other categories in 25. With regard to the cures of brain infarction in the acute phase, direct percutaneous transluminal angioplasty (direct PTA) was carried out on three patients with atherothrombotic infarction, immediate PTA on two, superselective fibrinolytic therapy on two, and STA-MCA anastomosis on three. In all, ten atherothrombotic patients (6.3%) were treated by acute surgical or endovascular therapy. On the other hand, superselective fibrinolytic therapy was carried out on 35 patients (30.7%) with cardioembolic infarction. There were no patients in the lacunar infarction group who were given acute surgical treatment. Neurological improvement after 24 hours was recognized in 4 patients (40%) of 10 with atherothrombotic infarction, and in 9 patients (25.7%) of 35 with cardioembolic infarction. However, symptomatic intracerebral hematoma was recognized in 4 patients (11.4%) with cardioembolic infarction. Indication for acute surgical or endovascular treatment for brain infarction was very limited because of the time factor from the onset to admission. It is suggested that neurosurgeons might enlighten citizens about the necessity for acute surgical or endovascular therapy for stroke.

Angioplasty, Balloon, Coronary↗
PubMed2003

Silent brain infarcts and white matter lesions increase stroke risk in the general population: the Rotterdam Scan Study.

BACKGROUND AND PURPOSE: Silent brain infarcts and white matter lesions are associated with an increased risk of subsequent stroke in minor stroke patients. In healthy elderly people, silent brain infarcts and white matter lesions are common, but little is known about their relevance. We examined the risk of stroke associated with these lesions in the general population. METHODS: The Rotterdam Scan Study is a population-based prospective cohort study among 1077 elderly people. The presence of silent brain infarcts and white matter lesions was scored on cerebral MRI scans obtained from 1995 to 1996. Participants were followed for stroke for on average 4.2 years. We estimated the risk of stroke in relation to presence of brain lesions with Cox proportional hazards regression analysis. RESULTS: Fifty-seven participants (6%) experienced a stroke during follow-up. Participants with silent brain infarcts had a 5 times higher stroke incidence than those without. The presence of silent brain infarcts increased the risk of stroke >3-fold, independently of other stroke risk factors (adjusted hazard ratio 3.9, 95% CI 2.3 to 6.8). People in the upper tertile of the white matter lesion distribution had an increased stroke risk compared with those in the lowest tertile (adjusted hazard ratio for periventricular lesions 4.7, 95% CI 2.0 to 11.2 and for subcortical lesions 3.6, 95% CI 1.4 to 9.2). Silent brain infarcts and severe white matter lesions increased the stroke risk independently of each other. CONCLUSIONS: Elderly people with silent brain infarcts and white matter lesions are at a strongly increased risk of stroke, which could not be explained by the major stroke risk factors.

Aged↗
PubMed1998

[Hemodynamics of asymptomatic brain infarction determined by Doppler sonography].

We compared the usefulness of two methods for diagnosing asymptomatic brain infarction: an ultrasonic quantitative flow measurement system (QFM) and a transcranial Doppler arteriography (TCDA). A total of 137 patients (73 men and 64 women) who underwent magnetic resonance imaging of the brain, QFM, and TCDA were enrolled. Their ages ranged from 41 to 83 years (mean age, 63 years). The patients were divided into 3 groups: 45 without cerebrovascular disease (Group N); 40 with asymptomatic brain infarction (Group AS); and 52 with lacunar infarction (Group LI). The mean blood flow in the common carotid artery (CCA-BF) was measured by QFM. The mean blood velocity and Fourier pulsatility index in the middle cerebral artery (MCA-BV, MCA-PI) were measured by TCDA. In Group N, 28 patients were examined twice at a mean interval of 2 years; 19 remained without asymptomatic brain infarction (Group N1), and asymptomatic brain infarction developed in the remaining 9 (Group N2). The 3 groups differed significantly in MCA-PI (N < AS < LI), but not in CCA-BF or in MCA-BV. The MCA-PI in Group N2 was higher than that in Group N1. These results indicate that the Fourier pulsatility index determined by TCDA may be useful for detecting the onset of asymptomatic brain infarction.

Adult↗
PubMed1996

[Lacunar brain infarction in patients with pseudoxanthoma elasticum].

Brain infarctions in patients with pseudoxanthoma elasticum (PXE) are thought to be associated with the damage of cerebral arteries injured by connective tissue change caused by PXE. We experienced 3 cases of PXE with lacunar brain infarction and evaluated the relationship between the damage of small penetrating arteries and PXE. All patients' diagnosis of PXE were confirmed by histological examination. They were a 47-year-old man and two women with 54 and 62 years of age old. All patients had pseudoxanthoma and angioid streaks and showed pyramidal tract signs. In addition, one patient presented Parkinsonism and another presented involuntary movement of the left lower extremities. None of these cases showed cortical symptoms. Brain CT and MRI revealed multiple lacuna in the areas of penetrating arteries, but their cerebral angiogram were almost normal. Severe small artery diseases, which cannot be attributable only to hypertension, were present. The relationship between such severe small artery disease and damage of the origin of small penetrating arteries caused by PXE was strongly suggested.

Dementia, Multi-Infarct↗
PubMed2002

Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study.

BACKGROUND AND PURPOSE: Silent brain infarcts are commonly seen on magnetic resonance imaging (MRI) both in patients with a first stroke and in healthy elderly persons. These infarcts seem associated with an increased risk of stroke. It is unclear whether risk factors for silent infarcts differ from those for symptomatic stroke. We investigated the prevalence of, and cardiovascular risk factors for, silent brain infarcts. METHODS: The Rotterdam Scan Study is a population-based cohort study among 1077 participants 60 to 90 years of age. Participants underwent cerebral MRI. We assessed cardiovascular risk factors by interview and physical examination. Associations between risk factors and presence of infarcts were analyzed by logistic regression and adjusted for age, sex, and relevant confounders. RESULTS: For 259 participants (24%) 1 or more infarcts on MRI were seen; 217 persons had only silent and 42 had symptomatic infarcts. The prevalence odds ratio (OR) of both silent and symptomatic infarcts increased with age by 8% per year (95% CI, 1.06 to 1.10 and 1.04 to 1.13, respectively). Silent infarcts were more frequent in women (age-adjusted OR, 1.4; 95% CI, 1.0 to 1.8). Hypertension was associated with silent infarcts (age- and sex-adjusted OR, 2.4; 95% CI, 1.7 to 3.3), but diabetes mellitus and smoking were not. CONCLUSIONS: Silent brain infarcts are 5 times as prevalent as symptomatic brain infarcts in the general population. Their prevalence increases with age and seems higher in women. Hypertension is associated with silent infarcts, but other cardiovascular risk factors are not.

Age Factors↗
PubMed1997

Brain infarction and the clinical expression of Alzheimer disease. The Nun Study.

OBJECTIVE: To determine the relationship of brain infarction to the clinical expression of Alzheimer disease (AD). DESIGN: Cognitive function and the prevalence of dementia were determined for participants in the Nun Study who later died. At autopsy, lacunar and larger brain infarcts were identified, and senile plaques and neurofibrillary tangles in the neocortex were quantitated. Participants with abundant senile plaques and some neurofibrillary tangles in the neocortex were classified as having met the neuropathologic criteria for AD. SETTING: Convents in the Midwestern, Eastern, and Southern United States. PARTICIPANTS: A total of 102 college-educated women aged 76 to 100 years. MAIN OUTCOME MEASURES: Cognitive function assessed by standard tests and dementia and AD assessed by clinical and neuropathologic criteria. RESULTS: Among 61 participants who met the neuropathologic criteria for AD, those with brain infarcts had poorer cognitive function and a higher prevalence of dementia than those without infarcts. Participants with lacunar infarcts in the basal ganglia, thalamus, or deep white matter had an especially high prevalence of dementia, compared with those without infarcts (the odds ratio [OR] for dementia was 20.7, 95% confidence interval [95% CI], 1.5-288.0). Fewer neuropathologic lesions of AD appeared to result in dementia in those with lacunar infarcts in the basal ganglia, thalamus, or deep white matter than in those without infarcts. In contrast, among 41 participants who did not meet the neuropathologic criteria for AD, brain infarcts were only weakly associated with poor cognitive function and dementia. Among all 102 participants, atherosclerosis of the circle of Willis was strongly associated with lacunar and large brain infarcts. CONCLUSION: These findings suggest that cerebrovascular disease may play an important role in determining the presence and severity of the clinical symptoms of AD.

Aged↗
PubMed2002

A phosphodiesterase inhibitor, cilostazol, prevents the onset of silent brain infarction in Japanese subjects with Type II diabetes.

AIMS/HYPOTHESIS: This study aimed to evaluate the effect of a phosphodiesterase inhibitor, cilostazol, on the prevention of silent brain infarction in diabetic patients without symptoms of vascular events. METHODS: A total of 89 subjects were allocated at random to the cilostazol group ( n = 43) or the control group ( n = 46). RESULTS: After the study period (3.2 +/- 0.5 years), carotid intima-media thickness (IMT) (means +/- SD) had increased ( p < 0.01) by 0.18 +/- 0.19 mm in the control group. In the cilostazol group, intima-media thickness showed almost no change (-0.00 +/- 0.16 mm). In the control group, 2 out of 46 subjects showed symptomatic brain infarctions and 10 out of 34 subjects without infarct-like region assessed by standard brain MRI examination showed silent brain infarctions after the observation period. On the other hand, no subjects in the cilostazol group showed silent brain infarction or strokes during the study period. Both at the beginning and end of the study period, the number of infarct-like regions positively correlated with IMT ( r = 0.335, p < 0.001 or r = 0.347, p < 0.001 respectively). The progression of infarct-like regions was directly related to the increase in IMT during the study period ( r = 0.299, p = 0.004). CONCLUSION/INTERPRETATION: These data demonstrated that cilostazol could prevent the onset of silent brain infarction in Japanese subjects with Type II (non-insulin-dependent) diabetes mellitus. Also, an increase in intima-media thickness of the carotid artery wall could be able to predict the onset of silent brain infarction.

Aged↗