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PubMed1989

[Arrhythmia in patients with cerebral infarction evaluated by Holter ECG].

In the present study, Holter ECG (24 hours continuous monitoring) was applied for detection of arrhythmia in patients with cerebral infarction to elucidate the relationship between arrhythmias and types of cerebral infarction. The subjects were 111 patients (80 males and 31 females) with cerebral infarction who were admitted to our institution during the acute stage. Their average age was 65.4 years old. They were divided into the following three groups: Group L; patients having a large low density area on CT including the cortex, group S; those having a small low density area in the basal ganglia, and group N; those having no low density area on CT. Holter ECG was taken at least three weeks after onset in all cases. Fourteen of them were also examined in the acute stage, and these findings were compared with those taken in the chronic stage. Three Holter ECGs recorded incidentally before the onset of stroke were used for comparison. Based on the basic rhythms recorded on the Holter ECG, the subjects were divided into sinus rhythm and atrial fibrillation cases. The total number of ventricular premature contractions (VPCs), were determined in each case. There was little difference in the number of total VPCs among the records taken in the pre-onset, acute and chronic stages. There also was no relation between the total number of VPCs and the age, history of hypertension, and the site of infarction on CT. There was no consistent relationship between the total number of VPCs in cases with atrial fibrillation and CT findings.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2000

[Clinical study on ultra-early intravenous thrombolysis with high-dose urokinase in treatment of acute cerebral infarction].

OBJECTIVE: To determine the clinical curative effect and safety of ultra-early intravenous thrombolysis with high-dose urokinase in treatment of acute cerebral infarction. METHODS: Thirty-one patients with atherosclerotic cerebral infarction were treated with a single dose of 1.5 x 10(4) U/kg urokinase as intravenous thrombolytic therapy within 6 h after the onset. The decrease degree of nerve function defect integral, the cure rate, the effectual rate, and the total effective rate were observed 3 h and 21 days after thrombolysis, respectively, and the results were compared with those of conventional treatment. The infarct volume of patients treated with the two therapies were compared 21 days after treatment. RESULTS: The nerve function defect integral examined 3 h after thrombolysis (14.2 +/- 2.1) was markedly lower than that before thrombolysis (26.5 +/- 9.1). A remarkable difference (n = 31, t = 4.669, P < 0.05) was noticed between them. The cure rate and effectual rate reached 22.58% (7/31) and 67.74% (21/31), respectively. The decrease degree of nerve function defect integral, the cure rate, the effectual rate and the total effective rate evaluated 21 days after thrombolysis were all higher than those of conventional therapy group (from 26.5 +/- 9.1 to 8.8 +/- 2.8 vs from 26.4 +/- 8.1 to 16.3 +/- 4.1, t = 2.417; 51.61% vs 15. 38%, chi(2) = 5.037; 70.96% vs 42.30%, chi(2) = 4.765; 87.09% vs 65.38%, chi(2) = 3.886, respectively; all P < 0.05). The infarct volume was markedly smaller than that of the conventional therapy group (3.7 cm 3 +/- 3.0 cm(3) vs 5.3 cm(3) +/- 3.1 cm(3), t = 2.165, P < 0.05). CONCLUSION: Ultra-early intravenous thrombolysis with a single dose of 1.5x10(4) U/kg urokinase in the treatment of atherosclerotic cerebral infarction has a better clinical curative effect and less complication, and it can also have the infarct volume markedly reduced.

Cerebral Infarction↗
PubMed2001

Spironolactone reduces cerebral infarct size and EGF-receptor mRNA in stroke-prone rats.

Remodeling of the cerebral vasculature contributes to the pathogenesis of cerebral ischemia. Remodeling is caused by increased smooth muscle proliferation and may be due to an increase in the responsiveness of vascular cells to epidermal growth factor (EGF). Aldosterone is a risk factor for stroke, and the literature suggests it may play a role in increasing the expression of the receptor for EGF (EGFR). We hypothesized that mRNA for the EGF-stimulated pathway would be elevated in the vasculature of stroke-prone spontaneously hypertensive rats (SHRSP) and that this and experimental ischemic cerebral infract size would be reduced by aldosterone inhibition with spironolactone. We found that spironolactone treatment reduced the size of cerebral infarcts after middle cerebral artery occlusion in SHRSP (51.69 +/- 3.60 vs. 22.00 +/- 6.69% of hemisphere-infarcted SHRSP vs. SHRSP + spironolactone P < 0.05). Expression of EGF and EGFR mRNA was higher in cerebral vessels and aorta from adult SHRSP compared with Wistar-Kyoto rats. Only the expression of EGFR mRNA was elevated in the young SHRSP. Spironolactone reduced the EGFR mRNA expression in the aorta (1.09 +/- 0.25 vs. 0.56 +/- 0.11 phosphorimage units SHRSP vs. SHRSP + spironolactone P < 0.05) but had no effect on EGF mRNA. In vitro incubation of aorta with aldosterone +/- spironolactone produced similar results, suggesting a direct effect of aldosterone. Thus spironolactone may reduce the size of cerebral infarcts via a reduction in the expression of the EGFR mRNA, leading to reduced remodeling.

Aldosterone↗
PubMed1996

Visual function and perinatal focal cerebral infarction.

AIMS: To evaluate the visual function of infants with perinatal cerebral infarction in whom the site and size of the lesion has been determined using magnetic resonance imaging (MRI). METHODS: Twelve infants with cerebral infarction on MRI were studied with a battery of tests specifically designed to evaluate visual function in infancy. This included tests: for visual attention (fixation shifts); of cerebral asymmetry (optokinetic nystagmus, visual fields); for assessment of acuity (forced choice preferential looking); and neurophysiological measures of vision (phase reversal and orientation reversal visual evoked potential). RESULTS: A considerable incidence of abnormalities on at least one of the tests for visual function used was observed. The presence or severity of visual abnormalities could not always be predicted by the site and extent of the lesion seen on imaging. CONCLUSIONS: Early focal lesions affecting the visual pathway can, to some extent, be compensated for by the immature developing brain. These data suggest that all the infants presenting with focal lesions need to be investigated with a detailed assessment of various aspects of vision.

Cerebral Infarction↗
PubMed2000

Pravastatin use and risk of coronary events and cerebral infarction in japanese men with moderate hypercholesterolemia: the Kyushu Lipid Intervention Study.

The Kyushu Lipid Intervention Study (KLIS) aimed to investigate the effects of pravastatin in the primary prevention of coronary events and cerebral infarction in Japanese men aged 45-74 years with serum total cholesterol of > or = 220 mg/dl (5.69 mmol/l). The coronary events included myocardial infarction, coronary artery surgery and angioplasty, cardiac death, and sudden death. A total of 5,640 patients were recruited, and 3,061 and 2,579 were allocated to the pravastatin (10-20 mg/day) and conventional treatment, respectively. They were followed up for 5 years on average. Due to unsuccessful randomization, a protocol-based analysis was carried out with adjustment for coronary risk factors at baseline using the Cox proportional hazards model. For several reasons (serum total cholesterol of > or = 300 mg/dl, use of drugs excluded in protocol, etc.), 2,219 men in the pravastain group and 1,634 in the conventional treatment group were used in the analysis. The baseline total cholesterol levels were 254 mg/dl in the pravastain group and 243 mg/dl in the conventional treatment group. Serum total cholesterol levels fell by 15% in the pravastain group and by 8% with the conventional treatment group. Adjusted relative risks for pravastatin versus conventional treatment were: coronary events 0.86 (one-side p=0.23), cerebral infarction 0.78 (p=0.13), and the two outcomes combined 0.81 (p=0.08). These findings add to evidence that pravastatin use is beneficial in the prevention of coronary events and cerebral infarction in hypercholesterolemic Japanese patients, and suggest that pravastatin may be more protective against cerebral infarction.

Aged↗
PubMed1996

Plasma beta-hexosaminidase isoenzymes A and B in patients with cerebral infarction.

We determined plasma activity of the isoenzymes of beta-hexosaminidase (Hex) in 151 patients with cerebral infarction, since earlier findings have shown a relation between Hex isoenzymes and risk factors for vascular disease in normal subjects. Compared with 206 control subjects, an elevated level of plasma Hex isoenzymes was found in patients with cerebral infarction, particularly females. However, there was no relation to the clinical subtypes of diagnosis or to the presence of any risk factors for vascular disease, such as carotid artery stenosis, major potential cardio-embolic risk factors on echocardiography, hypertension, heart disease, diabetes mellitus or tobacco smoking. Instead, our findings indicate that Hex isoenzymes in patients with cerebral infarction are more influenced by the level of serum aspartate aminotransferase and blood glucose. The main conclusion is that the liver function as reflected by the level of liver enzymes and glucose metabolism are the major determinants of Hex isoenzymes in plasma.

Aged↗
PubMed1996

Asymptomatic cerebral infarctions in patients with ischemic stroke.

We studied 383 consecutive patients with stroke and ischemic lesions on CT scan for the presence of symptomatic cerebral infarction (SCI) and asymptomatic cerebral infarction (ACI). We evaluated risk factors as well as volume, site and number of the lesions. ACIs occurred in 34% of the cases (130/383); 88% of ACIs were lacunes and internal borderzone infarctions, with a volume of less than 2 ml. Larger infarctions were asymptomatic in 27 patients (20.8%); 114 (68.7%) out of 166 patients with two or more SCIs (68.7%) had one or more ACIs. Infarctions in the lateral middle cerebral artery (MCA) territory were SCIs, in the medial MCA territory ACIs. Independent risk factors for ACI were age above 70 years and smoking; cardioembolism prevailed in SCI, small vessel disease in ACI; high levels of disability prevailed in SCIs.

Aged↗
PubMed1995

[The relationship among hematocrit, platelet aggregation and the time of onset in patients with acute stage-cerebral infarction].

We evaluated time relation among hematocrit (Ht), platelet aggregation (PA) and the onset of acute stage-cerebral infarction in 221 patients. Lacunar infarctions were likely to occur in the evening or at midnight. The elevated Ht value was frequently found in patients with infarctions occurring at midnight, suggesting that the elevation of blood viscosity has an intimate etiology to the onset. The decrease of PA was often found in those who suffered from their stroke while awake in the morning or at midnight, and frequently had been associated with elevated Ht in the latter patients. Decrease of PA is often reported during acute stage-cerebral infarction. Our results indicate that increased platelet aggregation may play an important role in developing cerebral infarction, especially in those who had onset of illness in the morning.

Acute Disease↗
PubMed2000

Mongolian gerbil (Meriones unguiculatus) as a model of cerebral infarction for testing new therapeutic agents.

Stroke mortality represents the third leading cause of death worldwide, after coronary artery disease and cancer. It has been demonstrated that in Mongolian gerbils, a unilateral hemispheric cerebral infarction can be produced following unilateral occlusion of the carotid artery because of the absence of connecting arteries between the basilar and carotid systems in these animals. The objective of this study was to comprehensively characterize the model of cerebral infarction in gerbil, clinically, biochemically and especially morphologically for prospective use in testing new therapeutic agents. Cerebral infarction was produced by ligation of the left common carotid artery in experimental gerbils. The control animals were sham-operated. One hour after surgery, 0.5 ml of 1% trypan blue was administered intraperitoneally to all animals. Initial clinical evaluations were made 8 h after surgery and every day thereafter for 30 days. On each of days 10 and 30, 4 animals were sacrificed. The degree of cerebral infarction was evaluated on the basis of clinical response, electrolyte and enzyme changes, vascular permeability of blood-brain barrier and morphological alterations. The total post-infarction mortality rate was 50%. The clinical symptoms presented as ipsilateral hemiparesis, ptosis of the eyelid, circling behavior, decreased breathing rate, decreased blood pressure and increased heart rate. Such symptoms developed within 8 h of ligation and persisted to sacrifice at day 30. Creatine kinase increased significantly on the 10th day and remained high to day 30. Increased potassium from the damaged cells and breakdown of the blood-brain barrier were first detected 72 h post-infarction. The morphological data showed evidence of brain cell necrosis, autolysis and phagocytosis 10 and 30 days post-ligation in left hemispheres. Minor intercellular edema and some cell shrinkage was evident in the right brain. Areas of focal necrosis in the vicinity of blood vessels, especially in the left brain suggested a reperfusion injury as a consequence of minimal collateral reflow from the right brain into the left brain microvasculature. Experimental infarction in gerbil recreates the ischemic conditions causing stroke in humans. The animal model may be used for evaluating the efficacy of therapeutic agents that may ameliorate the condition in man.

Animals↗
PubMed2005

[Effects of atorvastatin on plasma hypersensitive C-reactive protein and interleukin-6 in patients with acute cerebral infarction].

OBJECTIVE: To observe the effects of different doses of atorvastatin on the plasma hypersensitive C-reactive protein (hsCRP) and interleukin-6 (IL-6) in patients with acute cerebral infarction. METHODS: 131 patients with acute cerebral infarction, 73 males and 58 females, aged 63 +/- 11, were randomly divided into 3 groups: Group A (n = 47), with basal treatment; Group B (n = 42), atorvastatin 10 mg was added every night; and Group C (n = 42), atorvastatin 20 mg was added every night. Before the treatment and 7 and 14 days after the treatment the plasma levels of hsCRP and IL-6, fasting plasma levels of lipid, such as total cholesterol (TC) and low density lipoprotein-C (LDL-C), liver functions, such as aspartate aminotransferase (ALT) and alanine transaminase (ALT), creatine kinase (CK), urea nitrogen, were detected. Neurological function deficit was determined. The survival condition was surveyed 6 months after. RESULTS: (1) The TC and LDL-C decreased after treatment in the 3 groups with significant differences between Group A and Group C, Group B and Group C, and Group B and Group C (all P < 0.05). (2) The plasma level of hsCRP decreased by 9.1%, 33.9%, and 30.1% respectively 7 days after treatment in Groups A, B, and C with significant differences between Groups A and B and between Groups A and C (both P < 0.05), however, without significant difference between Group B and Group C. The level of hsCRP decreased by 34.3%, 56.0%, and 52.9% respectively 14 days after treatment in the 3 groups with significant differences between Groups A and B and between Groups A and C (both P < 0.05), however, without significant difference between Group B and Group C. (3) The level of IL-6 decreased 7 and 14 days after treatment in all 3 groups, however, without significant differences between any 2 groups (all P > 0.05). (4) The decrease of hsCRP and decrease of IL-6 were not correlated with the percentage of TC decrease (both P > 0.05) in Group B. The decrease of hsCRP was not correlated with the changes of blood lipids in Group C. (5) Both the plasma hsCRP and IL-6 before treatment were positively correlated with the infection volume and neurological function score (all P < 0.01). CONCLUSION: Atorvastatin has an anti-inflammatory action benefiting the alleviation of secondary inflammatory damaged in acute cerebral infarction that is independent of lipid lowering.

Adult↗
PubMed2002

[Effect of transcranial magnetic stimulation on rehabilitation of motor function in patients with cerebral infarction].

OBJECTIVE: To study the effect of transcranial magnetic stimulation (TMS) on the rehabilitation of motor function in patients with cerebral infarction. METHODS: Two hundred twenty and three patients with the initial attack of cerebral infarction were divided into three groups. (1) One hundred twenty and three patients were randomly further divided into rehabilitation subgroup (n = 63, aged 64.0 +/- 7.9, treated with TMS beginning from the 6 approximately 10 th day after onset) and control subgroup (n = 60, aged 63.5 +/- 7.9). (2) Sixty patients were divided into three subgroups according to the age: 35 approximately 55 (n = 11), 56 approximately 75 (n = 20), and over 76 (n = 30). (3) Forty patients aged 56 approximately 75 were further divided into two subgroups according to the timing of beginning of TMS: subgroup with TMS beginning within 3 months after the initial attack (n = 20) and subgroup with TMS beginning 3 months after the initial attack (n = 20). Except for TMS, the basic treatment was the same for all of the patients. TMS was given once a day for 14 days. Fugl-Meyer score, Barthel index, and central spinal cord motor conduction time (CMCT) were measured twice: just before treatment and after the 14th treatment. A difference less than 20 ms between CMCT values measured before and after TMS and failure to induce CMCT both before and after TMS were regarded as ineffective hess, and a difference more than 20 ms between CMCT values measured before and after TMS and a change from failure to induce CMCT were regarded as effective hess. RESULTS: The effective rate was 90.5% in the rehabilitation subgroup and 68.3% in the control group (P < 0.05). The Fugl-Meyer scores were 36.3 +/- 15.8 and 33.7 +/- 13.7 in the rehabilitation subgroup and control subgroup before treatment respectively (P > 0.05), and were 51.7 +/- 15.7 and 40.0 +/- 13.9 after treatment respectively (P < 0.01). The Barthel index were 39.6 +/- 15.8 and 40.0 +/- 14.9 in the two subgroups before treatment respectively (P > 0.05) and were 50.5 +/- 15.7 and 43.9 +/- 15.3 after treatment respectively (P < 0.05). The Fugl-Meyer scores before and after TMS were 35.8 +/- 11.3 and 61.6 +/- 18.6 in the subgroup aged 35 approximately 55 (P < 0.01), 33.5 +/- 14.0 and 49.2 +/- 16.0 in the subgroup aged 56 approximately 75 (P < 0.001), and 32.1 +/- 10.7 and 37.6 +/- 11.3 in the subgroup aged over 75 (P > 0.05). The Fugl-Meyer scores were 41.2 +/- 15.7 and 59.0 +/- 22.8 before and after TCM respectively in the subgroup with early TMS treatment (P < 0.01), and were 34.3 +/- 13.5 and 45.4 +/- 14.8 respectively in the subgroup with TMS beginning 3 months after the onset (P < 0.05). CONCLUSION: TMS is effective on the rehabilitation of motor function in patients with cerebral infarction. The effectiveness of TMS treatment depends on the age of the patients and timing of beginning treatment.

Adult↗
PubMed2002

Carotid plaques increase the risk of stroke and subtypes of cerebral infarction in asymptomatic elderly: the Rotterdam study.

BACKGROUND: Few studies have quantified the relation between carotid plaques and stroke in asymptomatic patients, and limited data exist on the importance of location of plaques or the association with subtypes of cerebral infarction. We investigated the relationship between carotid plaques, measured at different locations, and risk of stroke and subtypes of cerebral infarction in a population-based study. Methods and Results- The study was based on the Rotterdam Study and included 4217 neurologically asymptomatic subjects aged 55 years or older. Presence of carotid plaques at 6 locations in the carotid arteries was assessed at baseline. Severity was categorized according to the number of affected sites. After a mean follow-up of 5.2 years, 160 strokes had occurred. Data were analyzed using Cox proportional hazards regression. Plaques increased the risk of stroke and cerebral infarction approximately 1.5-fold, irrespective of plaque location. Severe carotid plaques increased the risk of nonlacunar infarction in anterior (RR 3.2 [95% CI, 1.1 to 9.7]) but not in posterior circulation (RR 0.6 [95% CI, 0.1 to 4.9]). A >10-fold increased risk of lacunar infarction was found in subjects with severe plaques (RR 10.8 [95% CI, 1.7 to 69.7]). No clear difference in risk estimates was seen between ipsilateral and contralateral infarction. CONCLUSIONS: Carotid plaques increase the risk of stroke and cerebral infarction, irrespective of their location. Plaques increase the risk of infarctions in the anterior but not in the posterior circulation. It is likely that carotid plaques in neurologically asymptomatic subjects are both markers of generalized atherosclerosis and sources of thromboemboli.

Aged↗
PubMed1988

Cardiopulmonary metastatic lesions of osteosarcoma and associated cerebral infarction.

Osteogenic sarcoma frequently disseminates by hematogenous routes. A 32-year-old patient underwent evaluation for an acute cerebral infarction. Cardiac auscultation disclosed an abnormal diastolic sound. Echocardiographic examination revealed a large left atrial mass, which was found at thoracotomy to be metastatic osteogenic sarcoma. Cerebral computed tomographic scans at the time of initial examination and 3 months later demonstrated new cerebral lesions consistent with metastatic growths. The abrupt cerebral infarction, other clinical findings, and results of diagnostic studies strongly suggested that the acute cerebrovascular event was the result of metastatic cerebral embolization from the tumor material found in the thorax. Cerebral infarction is an unusual and catastrophic complication of thoracic metastatic lesions of osteogenic sarcoma.

Adult↗
PubMed1993

Post-operative cerebral infarction and Takayasu's disease.

A case of post-operative cerebral infarction is presented in a 53-year-old man, in whom a clinical diagnosis of Takayasu's disease was made retrospectively. The cerebral infarction occurred in the absence of any identifiable surgical or anaesthetic cause. The possible role of sodium nitroprusside in preventing cerebrovascular accidents in this condition is discussed and the literature reviewed.

Cerebral Infarction↗
PubMed1993

Cerebral infarction following thoracic herpes zoster.

OBJECTIVE: To present a case of cerebral infarction following thoracic herpes zoster presenting as Gerstmann's syndrome. CLINICAL FEATURES: A 61 year old male developed herpes zoster of T 1-2 dermatomes. Four months later he developed a confusional state together with expressive aphasia, dyscalculia, dysgraphia and finger agnosia with no long tract signs. CT scan of head showed recent infarction of this left parietal lobe. He received a five day course of acyclovir 800 mg four times daily and showed slow but steady improvement. CONCLUSION: Herpes zoster is uncommonly followed by cerebral infarction. Acyclovir may have a role in therapy of this complication.

Acyclovir↗
PubMed1986

Cerebral infarction in Hemophilus influenzae type B meningitis.

Over a 5-year period, 8 (4.7%) of the 170 children diagnosed at Milwaukee Children's Hospital as having Hemophilus influenzae type b (HITB) meningitis developed cerebral infarction. Compared with children who did not develop infarcts or with children who developed other neurologic complications, such as subdural effusion, empyema, or meningoencephalitis, these children had significantly higher cerebrospinal fluid (CSF) leukocyte counts on initial lumbar puncture and had a greater likelihood of seizure activity. In seven of eight patients with cerebral infarction, a focal or generalized seizure heralded neurologic findings associated with abnormal radiographic studies. Two of the eight patients died, and two were permanently severely damaged. In the other four patients, there was eventual recovery from gross neurologic deficits. The mortality in patients with HITB meningitis complicated by cerebral infarction (25%) was significantly greater than that in other patients with HITB meningitis (0.6%). The pathophysiology of infarction in patients with bacterial meningitis is uncertain but may in part relate to arteriospasm. Cerebral infarction is a serious, and in the present experience, not uncommon complication of H. influenzae meningitis.

Cerebral Infarction↗
PubMed2003

Homocysteine and cerebral infarction in finnish male smokers.

BACKGROUND AND PURPOSE: Homocysteine is associated with stroke, but it is not clear whether this relationship is causal. We examined the association between total serum homocysteine concentration (tHcy) and cerebral infarction in a cohort of Finnish male smokers. METHODS: This is a matched case-control study of 201 cases of cerebral infarction and 201 concurrently sampled age-matched controls nested in a cohort of 13 840 male smokers free of cardiovascular disease at the completion of the Alpha-Tocopherol and Beta-Carotene (ATBC) Cancer Prevention study. Conditional logistic regression was used to calculate odds ratios (ORs) and to adjust for confounding variables. An unmatched analysis was also performed. RESULTS: The geometric mean tHcy was 13.3 micromol/L (95% CI, 12.6 to 13.9) in cases and 12.6 micromol/L (95% CI, 12.0 to 13.2) in controls (P=0.09). There was a graded increase in the OR of cerebral infarction per quartile increase in tHcy (OR, 1.0, 1.7, 1.9, 2.1; trend P=0.02; 201 case-control pairs) when adjusted for traditional risk factors. There was a similar trend in a subgroup of 120 case-control pairs for which further adjustment for lifestyle factors was possible (OR, 1.0, 1.9, 2.5, 2.2; trend P=0.07 in the matched analyses; OR, 1.0, 1.2, 1.9, 2.0; trend P=0.02 in the unmatched analyses). The adjusted OR per 1-SD increase in log-transformed tHcy (equivalent to 4.7 micromol) was 1.4 (95% CI, 1.1 to 1.7; P=0.01). CONCLUSIONS: tHcy appears to predict cerebral infarction in Finnish male smokers.

Aged↗
PubMed1986

The association between the lupus anticoagulant and cerebral infarction in systemic lupus erythematosus.

The lupus anticoagulant (LAC) is associated with the occurrence of thromboembolic complications. Assuming that thrombosis may underlie manifestations of the central nervous system (CNS) in patients with systemic lupus erythematosus (SLE), we studied 20 patients with SLE and CNS manifestations for the presence of LAC. In 8 patients (40%) including 4 with overt cerebral infarction, LAC was demonstrated. The 4 patients with LAC and cerebral infarction all had thrombocytopenia, 2 had a history of peripheral thrombosis, and one recurrent abortion. In the 4 LAC-positive patients without overt cerebral infarction, thrombocytopenia was present in 3, a history of thrombosis in 2, and fetal wastage in one. We conclude that LAC identifies within the CNS-SLE group a subpopulation of patients in whom CNS manifestations are caused by cerebral infarction. This subpopulation is further characterized by increased prevalence of thrombocytopenia, peripheral thrombosis and fetal wastage. A possible pathogenetic role of LAC may be related to a hypercoagulable state occurring in this subgroup of SLE patients.

Adolescent↗