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The case of a patient who came to the Nuclear Medicine Department for a bone scintigraphy to rule out bone metastasis because of a lung neoplasm is presented. Some days before, the patient had suffered a right brain infarction. 99mTc-MDP uptake could be seen in the infarction area. Different mechanisms of 99mTc phosphates deposition in tissues other than bones are reviewed in this article.
MRI perfusion studies have focussed mainly on acute ischaemia and characterisation in ischaemia. Our purpose was to analyse regional brain haemodynamic information in acute, subacute, and chronic ischaemia. We performed 16 examinations of 11 patients on a 1.5 T MR images. Conventional and dynamic contrast-enhanced imaging were employed in all examinations. For the dynamic susceptibility sequences, a bolus (0.2 mmol/kg) of gadopentetate dimeglumine was injected. Reconstructed regional relative cerebral blood volume (rCBV) maps, bolus maps, and conventional images were analysed by consensus reading. In all examinations decreases in rCBV were observed in the lesions. The distribution of regional rCBV in lesions was heterogeneous. The rCBV of the periphery of the lesions was higher than that at their center. There was a correlation between the time since onset and abnormalities on the rCBV map and T2-weighted images (T2WI). In the early stage of acute stroke, the abnormalities tended to be larger on the rCBV than on T2WI. Many patterns of bolus passage were observed in ischaemic regions. rCBV maps provide additional haemodynamic information in patients with brain infarcts.
Independent risk factors for new atherothrombotic brain infarction (ABI) in older African-American men were hypertension (risk ratio 4.381), diabetes mellitus (risk ratio 2.872), and previous ABI (risk ratio 1.904). Independent risk factors for new coronary events in older African-American women were cigarette smoking (risk ratio 2.754), hypertension (risk ratio 5.914), diabetes mellitus (risk ratio 3.464), serum total cholesterol (risk ratio 1.008), serum high-density lipoprotein cholesterol (inverse association) (risk ratio 0.958), age (risk ratio 1.026), and previous ABI (risk ratio 2.601).
We report a 45-year-old woman with arrhythmogenic right ventricular dysplasia (ARVD). Because of congestive heart failure and atrial fibrillation, she underwent tricuspid valvular replacement and warfarin was prescribed. She suddenly had dysarthria, left hemiparesis and left hemispatial neglect. After brain CT examination, and cerebral angiography, she was diagnosed as cardiogenic brain embolism and infusion of low molecular heparin was started. On day 25, she suddenly had ventricular tachycardia and died in spite of treatment for arrhythmia. This is the first report of the case of cardiogenic brain embolism following ARVD. In this type of case, we must take care of arrhythmia besides the management of atrial fibrillation and brain infarction.
BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) is superior to conventional MRI in identification of small new ischemic lesions and discrimination of recent infarcts from old ones. Thus, this technique is useful in the detection of acute multiple brain infarcts (AMBI). We sought to determine the frequency and the topographical and etiologic patterns of AMBI detected on DWI. METHODS: We studied 329 consecutive ischemic stroke patients who underwent DWI and MRI/MR angiography within 4 days of stroke onset. AMBI was defined as noncontiguous high signal intensities on DWI in >1 vascular territory. Stroke mechanism was determined according to the criteria of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). RESULTS: We detected AMBI in 95 patients (28.9%). AMBI in anterior circulation was found in 62 cases: in 1 hemisphere in 42 (group A) and in bilateral hemispheres in 20 (group B). Twenty-two patients had AMBI in the posterior circulation (group C) and 11 in both anterior and posterior circulations (group D). The most frequent cause of stroke was large-artery atherosclerosis in groups A (33/42), B (9/20), and C (15/22) (P=0.02) and cardioembolism in group D (6/11) (P=0.02). Elevated fibrinogen or hematocrit was significantly associated with group B (P=0.01). In 9 patients in groups B and D, anatomic variations of anterior or posterior cerebral arteries or patent posterior communicating artery contributed to AMBI. CONCLUSIONS: Different topographical patterns of AMBI are associated with different vascular pathologies and stroke mechanisms. Hemorheologic abnormality or vascular anatomic variations may be contributing factors in the pathogenesis of AMBI in bilateral cerebral hemispheres or in both anterior and posterior circulations.
Entry of plasma proteins into damaged neurons has previously been demonstrated in various pathological conditions, but little is known about brain infarcts in this respect. In the present study, focal ischemic lesions were produced in rats by permanent occlusion of the middle cerebral artery (MCA). The animals were killed from 1 to 48 h postlesion. Leakage of plasma proteins across the blood-brain barrier into the infarcted area was visualized with immunostaining 2-3 h after the occlusion. This is earlier than in most previous reports. Entry of plasma proteins into ischemic neurons was seen 3 h after permanent occlusion of the MCA, while reliable changes were not seen until 12-24 h in sections stained with hematoxylin and eosin (H & E). Ischemic neurons stained for plasma proteins irrespective of their morphological appearance. Even cells that appeared normal with H & E staining were positively labeled. The technique may be used to diagnose very early ischemic lesions.
Factor XIII catalyzes the formation of covalent bounds between fibrin monomers, thus stabilizing the fibrin clot and increasing its resistance to fibrinolysis. The frequency of a frequent Val34Leu polymorphism in the FXIII A-subunit gene has been shown to be lower in patients with myocardial infarction or venous thrombosis than in controls, whereas it was higher in patients with hemorrhagic stroke than in controls. Our aim was to study the relation between brain infarction (BI) and the FXIII Val34Leu polymorphism in 456 patients consecutively recruited with a BI confirmed by MRI, and 456 matched controls. The distribution of genotypes was different in cases (63. 2% Val/Val; 30.9% Val/Leu; 5.9% Leu/Leu) compared with controls (49. 8% Val/Val; 42.8% Val/Leu; 7.4% Leu/Leu; P <.001). Carrying the Leu allele was associated with an OR of 0.58 (95% CI = 0.44-0.75). A similar association was observed in cases and controls free of previous cardiovascular or cerebrovascular history (OR = 0.51; 95% CI = 0.36-0.73). No heterogeneity of this association was observed after stratification on the main BI subtypes. Adjustment for traditional vascular risk factors did not modify these findings. In addition, the effect of smoking was modified by the polymorphism (P =.05); the effect of smoking was weaker among Leu carriers than among noncarriers. In conclusion, there was a negative association of the FXIII Val34Leu polymorphism with BI, thus suggesting a protective effect of the Leu allele against thrombotic cerebral artery occlusion. In addition, our results suggest that among Leu carriers, the protective effect of the polymorphism outweighed the effect of smoking. (Blood. 2000;95:586-591)
The purpose of this study was to determine the efficacy of diffusion-weighted imaging (DWI) and magnetization transfer imaging (MTI) in the differential diagnosis of brain infarct, infection, hamartoma, and tumor in 106 children. The apparent diffusion coefficients (ADCs) and magnetization transfer ratios (MTRs) of the lesions were compared using nonparametric tests. There was an inverse relationship between ADC and MTR in subacute/chronic infarct, infection, hamartoma, arachnoid cyst, and tumor relative to normal brain parenchyma. Both ADC and MTR were reduced in acute infarct. DWI and MTI had a complementary role in the differential diagnosis of acute infarct from infection with lower MTR, from hamartoma with higher ADC, and from low-grade gliomas and benign tumors that had higher ADCs and lower MTRs. ADCs increased and MTRs decreased with the duration of infarct and lower tumor grade.
BACKGROUND AND PURPOSE: Increased soluble thrombomodulin (sTM) concentration has been associated with recurrent coronary events, whereas in one prospective study it predicted fewer first-ever coronary events. One study found no relationship between brain infarction (BI) and sTM levels. Among all subjects of the Etude du Profil Génétique de l'Infarctus Cérébral (GENIC) cohort and those free of previous vascular history, we investigated the relationship between sTM level and BI risk, and among cases, its relationship with BI prognosis. METHODS: Patients with BI (n=492) were consecutively recruited from 12 centers. Hospital controls without a history of stroke (n=492) were individually matched for age, sex, and center. Blood samples were collected after hospitalization. Determination of sTM levels was centralized in a single laboratory. RESULTS: Soluble TM concentration significantly increased with age and hypertensive status, but was similar in cases and controls. With analyses restricted to 278 pairs of subjects with no previous vascular history, sTM concentration >59.6 microg/L (second and third tertiles compared with the first) was associated with fewer first-ever BI (adjusted odds ratio of 0.56 (95% CI, 0.35 to 0.89; P=0.014). Among the cases, increased sTM concentration was associated with a higher death rate after a median follow-up of 5.2 (1.4 to 6.4) years. The adjusted hazard ratio per 1 SD of sTM concentration increase (34.2 microg/L) was 1.19 (95% CI, 1.02 to 1.39; P=0.028). CONCLUSIONS: Increased sTM concentration may be protective against BI in subjects with no previous vascular disease, whereas it may predict a fatal outcome in patients who have already had a BI. Consequently, sTM levels should be interpreted according to vascular history.
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BACKGROUND AND PURPOSE: Nitric oxide (NO) synthesized by endothelial constitutive NO synthase (ecNOS) plays a key role in vascular regulation and atherosclerosis. Little is known concerning the role of the ecNOS gene (NOS3) as a risk factor for brain infarction (BI). Our aim was to investigate the relation between the Glu298Asp polymorphism in exon 7 of NOS3 with BI and its subtypes. METHODS: Patients (n=460; cases) with BI were consecutively recruited and classified into etiological subtypes. Control subjects (n=460; controls) without a history of stroke were recruited among individuals hospitalized at the same institutions and individually matched on age, sex, and center. Genotypes of the polymorphism were determined by polymerase chain reaction. RESULTS: The distribution of genotypes was significantly different between cases and controls (P=0.008); the GG genotype was more frequent in cases (46.1%) than in controls (35.4%; OR, 1.56; 95% CI, 1.19 to 2.04). Among subtypes, the frequency of the GG genotype was significantly higher in cases than in controls in the lacunar subtype (OR, 2.00; 95% CI, 1.05 to 3. 80); in this group, the relation between BI and LDL level was stronger among carriers of the GG genotype than among noncarriers (P for interaction, 0.05). CONCLUSIONS: Homozygosity for the G allele of the Glu298Asp polymorphism in NOS3 was associated with BI, and especially with lacunar stroke. Our findings suggest that genetic susceptibility and LDL cholesterol have a synergistic relation. Although these findings should be replicated in a larger sample of subjects and the functionality of the Glu298Asp polymorphism has not been established, these results may help us to understand the cause of the arteriolopathy underlying lacunae and have future implications in their treatment and prevention.
We examined brains clinicopathologically from 54 consecutive paroxysmal atrial fibrillation (PAF) patients aged 70 years or older and compared them with those of 59 age-matched controls. Symptomatic cerebral infarctions were present in 29 PAF patients (53.7%) and in 13 controls (22.0%) (p < 0.001). Symptomatic brain infarction was 2.4 times more common in PAF cases than in PAF-free controls; approximately 60% of the infarctions in the PAF cases were judged to be cardioembolic in origin. PAF in the elderly can be an important cause for cardiogenic cerebral embolism.
BACKGROUND: We report the prevalence and incidence of atherothrombotic brain infarction (ABI) in older Hispanic men and women in a long-term health care facility. METHODS: The prevalence and incidence of ABI and the association of risk factors with new ABI were investigated in 201 Hispanic men, mean age 79 +/- 8 years, and in 302 Hispanic women, mean age 80 +/- 9 years, in a long-term health care facility. Mean follow-up was 42 +/- 20 months in men and 47 +/- 26 months in women. RESULTS: The prevalence of prior ABI was 33% in Hispanic men and 30% in Hispanic women. The incidence of new ABI was 24% in Hispanic men and 23% in Hispanic women. Significant independent risk factors for new ABI were age (risk ratio = 1.09 in men and 1.08 in women for each increase of 1 year of age), current cigarette smoking (risk ratio = 2.8 in men and 2.7 in women), hypertension (risk ratio = 2.8 in men), diabetes mellitus (risk ratio = 3.5 in men and 5.0 in women), prior ABI (risk ratio = 5.6 in men and 5.5 in women), serum total cholesterol (risk ratio = 1.03 in men and 1.01 in women for each 1 mg/dl increase), and serum high-density lipoprotein (HDL) cholesterol (risk ratio = 1.06 in men and 1.06 in women for each 1 mg/dl decrease). CONCLUSIONS: Significant independent risk factors for new ABI were age, current cigarette smoking, diabetes mellitus, prior ABI, serum total cholesterol, and serum HDL cholesterol (inverse association) in older Hispanic men and women and hypertension in older Hispanic men.
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Various therapeutic methods have been attempted for cerebral infarction, but the development of more effective methods is still awaited. We have investigations of the effect of mannitol in preventing the development of cerebral infarction and have reported it effects in clinical cases of operated cerebral aneurysms. In recent years, our attention has been drawn to the so-called red cell substitute, perfluorochemicals (FC), which has a high oxygen-carrying capacity and a small particle less than 0.1 mu. In the present studies, using infarction models in dogs which have previously developed and reported, observations are made on the recovery of brain electrical activity in sever ischemia, suppressing brain swelling following recirculation of cerebral blood flow and protection upon the hemorrhagic brain infarction, due to administration of mannitol or FC. These experimental results indicate that the combined administration of mannitol and FC is effective in protecting the brain from cerebral ischemia.
This retrospective study was performed in order to evaluate the relationship between the risk of brain infarction and the severity of 274 internal carotid artery (ICA) stenoses in 218 patients. Clinical, vascular and brain-morphological findings were compared. Of 106 occluded ICAs, 59% had induced a completed stroke with visible hemispheric infarction in 77%, most of them of the territorial type (35%). 32% of 85 high-grade stenoses had led to completed strokes, with territorial, low-flow and microangiopathic patterns of infarction occurring equally frequent. CT was normal in two-thirds of 83 low-grade ICA-stenoses, whereas 14% showed microangiopathic brain lesions. We conclude that (1) asymptomatic ICA stenoses should not be operated on, as long as they are not of very high degree and (2) even symptomatic ICA stenoses should not undergo endarterectomy, if the patient's stroke was due to lacunar infarctions of typical site and size.
To investigate the role of superoxide in the toxicity of nitric oxide (NO), we examined the effect of nitric oxide synthase (NOS) inhibition on brain infarction in transgenic mice overexpressing CuZn-superoxide dismutase (SOD-1). Male SOD-transgenic mice and non-transgenic littermates (30-35 g) were subjected to 60 min of middle cerebral artery occlusion followed by 24 h of reperfusion. Either NG-nitro-L-arginine methyl ester (L-NAME; 3 mg/kg), a mixed neuronal and endothelial NOS inhibitor, or 7-nitroindazole (7-NI; 25 mg/kg), a selective neuronal NOS inhibitor, was administered intraperitoneally 5 min after the onset of ischemia. At 24 h of reperfusion, the mice were decapitated and the infarct volume was evaluated in each group. In the nontransgenic mice, L-NAME significantly increased the infarct volume as compared with the vehicle, while 7-NI significantly decreased it. In the SOD-transgenic mice, L-NAME-treated animals showed a significantly larger infarct volume than vehicle-treated ones, whereas there were no significant differences between 7-NI- and vehicle-treated mice. Our findings suggest that selective inhibition of neuronal NOS ameliorates ischemic brain injury and that both neuronal and endothelial NOS inhibition may result in the deterioration of ischemic injury due to vasoconstriction of the brain. Since L-NAME increased infarct volume even in SOD-transgenic mice, the protective effect of SOD could result from the vasodilation by increased endothelial NO as well as the reduction of neuronal injury due to less production of peroxynitrite compared to wild-type mice. Moreover, the neurotoxic role of NO might not be dependent on NO itself, but the reaction with superoxide to form peroxynitrite, because of no additive effects of SOD and a neuronal NOS inhibitor.