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PubMed1988

Acute cerebral infarction and changes of regional cerebral blow flow (rCBF) following experimental middle cerebral artery (MCA) occlusion.

An unanaesthetized cat model of acute focal cerebral ischaemia has been established by the technique of transorbital snare ligature for middle cerebral artery (MCA) occlusion. The model was used to investigate the patterns of changes of regional cerebral blood flow (rCBF) for up to 16 h following MCA occlusion by the hydrogen clearance technique and to explore the correlation among changes of rCBF, neurological deficits, and pathological changes. The animals were divided into 2 groups according to the size of infarct which was identified by 2% triphenyl tetrazolium chloride (TTC) solution stain. Infarct larger than 10% of coronal section surface of ipsilateral hemisphere was found in 18 cats (Group A), and a smaller infarct was found in the remaining 7 cats (Group B). Between these 2 groups, there was a statistically significant difference in the average rCBF value of the ipsilateral MCA territory. The increasing grade of contralateral paralysis correlated well with the decreasing rCBF in the ipsilateral MCA territory, and the increasing grade of cerebral hemispheric swelling was directly proportional to the increasing grade of paralysis. Three patterns of changes of rCBF were observed: persistent severe ischaemia (15 cats, Group A); persistent mild to moderate ischaemia (7 cats, Group B); and immediate severe ischaemia followed by early post-ischaemic hyperaemia and death (3 cats, Group A). During the initial stage of ischaemia, a significant decrease in rCBF of the contralateral hemisphere was observed in both groups, however, in Group A rCBF gradually increased to preocclusion level, while Group B presented a further decrease in rCBF suggesting the occurrence of interhemispheric diaschisis. Thus, Group B appeared to take advantage of diaschisis during the late phase of infarct development, as well as the substantial collateral flow from the surrounding anterior and posterior cerebral artery territories.

Animals↗
PubMed2003

Memory strategy training in children with cerebral infarcts related to sickle cell disease.

Cerebral infarcts occur in approximately 30% of children with sickle cell disease (SCD), but little information exists regarding remediation of associated cognitive deficits. The authors examined the benefits of training children with infarcts to use memory strategies. Six children with SCD-related infarcts received academic tutoring; three of these children received additional training in memory strategies (silent rehearsal to facilitate short-term memory and semantic organization to facilitate long-term memory). The performance of children receiving strategy training appeared to improve more than that of children receiving only tutoring. Memory in children with SCD-related infarcts may be enhanced through strategy training.

Adolescent↗
PubMed1992

Transesophageal echocardiographic detection of aortic arch disease in patients with cerebral infarction.

BACKGROUND AND PURPOSE: Ulcerated plaques in the aortic arch are frequent autopsy findings in patients with cerebral infarctions, particularly those of unknown cause. It has been suggested that they could be a source of cerebral emboli. Using transesophageal echocardiography, we prospectively studied 12 consecutive patients with cerebral infarction of undetermined cause after noninvasive workup to evaluate the frequency of aortic plaques or mural thrombi that could embolize in cerebral arteries. SUMMARY OF REVIEW: Six patients (50%) had an intraluminal echogenic mass of the aortic arch, mainly located at the junction of the ascending aorta and arch. This material was pedunculated (in one patient) or broad based (in five patients) with a markedly irregular surface and intraluminal extension from 3 to 15 mm. In addition, we found cholesterol emboli in two of the four patients who underwent quadriceps biopsy. CONCLUSIONS: These results show that transesophageal echocardiography has capabilities in detecting such lesions and point to the aortic arch as a possible source of cerebral emboli in patients with cerebral infarction of unknown cause.

Aged↗
PubMed1988

Sonography of cerebral infarction in infancy.

Six infants with cerebral infarcts were examined prospectively with real-time sonography to determine the sonographic characteristics of infarcts and their evolution. Patients' ages ranged from 1 day to 7 months, and serial sonographic and/or CT scans were obtained over a period of 2 weeks to 14 months in the survivors. Among our patients the most characteristic sonographic findings of infarction were absence of gyral definition, absence of vascular pulsations, altered parenchymal echogenicity, and territorial distribution. Mass effect, reflected in ventricular size and shift of midline structures, may also be seen and largely parallels the extent of the infarction. Evolution of infarcts was seen sonographically as gradual return of arterial pulsations and concurrent development of cystic spaces. Sonography was found to be a valuable tool in the diagnosis of infarction in infancy and in monitoring its evolution, although CT was necessary for adequate initial evaluation in older infants.

Brain↗
PubMed1994

Silent cerebral infarction associated with coronary artery disease.

To investigate the relationship of coronary artery disease and silent cerebral infarction, 50 patients who underwent coronary arteriography and cranial magnetic resonance imaging were studied. The patients were divided into three groups. The incidence of silent cerebral infarction (chiefly lacunar infarction) was significantly higher in patients with old myocardial infarction and in those with angina pectoris than in the control group (80, 78 and 29%, respectively, p < 0.05). Silent cerebral infarction is considered to be a risk factor for symptomatic cerebrovascular disease, so more attention should be focussed on the prevention of stroke in patients with coronary artery disease.

Aged↗
PubMedDate not supplied

MR imaging of acute cerebral infarction: experimental study with Gd-DTPA.

To evaluate the sensitivity of MR imaging for acute cerebral infarction and the effectiveness of MR enhancement with Gd-DTPA, we created a canine model of cerebral infarction by transarterial embolization (TAE). The external and internal carotid arteries were embolized respectively through a transfemoral catheter. MR imaging was performed with the Yokogawa Medical System prototype superconducting MR machine "Resona" operating at 0.35 Tesla. MR enhancement was done with 0.4 mmol/kg of Gd-DTPA. Early detectability without Gd-DTPA was 60% (3/5) two hours after TAE and 67% (4/6) at three hours. MR imaging showed high-intensity lesions on the T2-weighted sequence (SE 2000/100). The T1-weighted sequence (SR 250-600/25-35) did not reveal any lesions four hours after TAE. Five animals which received Gd-DTPA showed abnormal enhancement in the brain parenchyma within 30 min after Gd injection on the T1 weighted sequence. Gd-DTPA enhancement not only improved early sensitivity for acute cerebral infarction when MR imaging without Gd-DTPA was negative, but also enhanced the size and number of lesions compared with SE 2000/100 images without enhancement. The breakdown of the blood-brain barrier was suggested to be an important factor in Gd-DTPA enhancement.

Animals↗
PubMed1991

[Cerebral infarction: lacunae].

Lacunae are small deep cerebral infarcts which are believed to occur in hypertensive patients, producing characteristic clinical syndromes. Previous reports suggested to differentiate this type of stroke from other cerebrovascular diseases, but failed to provide any evidence that this classification is useful in clinical practice. We reviewed the present literature concerning pathogenesis, clinical features, diagnostic, and therapeutic aspects of lacunae and we established that current concepts in lacunar stroke are inadequately supported. Although lacunar syndromes are reported to be correlated with lacunar infarcts, these syndromes are also described in patients with different pathological findings. The assumption that lacunae always result from a distinct and specific small-vessel arteriopathy is not confirmed; in fact, an atheroma may occlude a single perforating artery at the base of the brain as well as larger arteries. Lipohyalinosis, initially referred to as the underlying pathologic vascular lesion specific for lacunae, is found most commonly in a subset of patients with severe hypertension associated with multilacunar dementia. Large infarcts and hemorrhages are reported to coexist with lacunae in autoptic and neuroradiological studies; intracranial atherosclerosis is associated with lacunae as well as with large superficial infarcts. The percentage of patients with hypertension is approximately the same regardless of type of the infarct, lacunar or cortical. Diagnostic criteria are not clear-cut: clinical onset, neurological examination, and assessment of risk factors are unable to take lacunae apart from other infarcts; the size of the lesion, but not the site or the pathogenesis, determines clinical course, degree of motor deficit, and prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed1980

[Cerebrospinal fluid glucose, lactate and pyruvate concentration in patients with cerebral infarction after intravenous glucose loading test].

The determinations of the above substances were done in the blood and CSF of 27 patients with cerebral infarction and 10 controls. The glucose level was determined in the blood and CSF and lactate and pyruvate levels in the CSF before and in the 8th and 16th minutes after a glucose load. The 0-toluidine colorimetric method was used for glucose and spectrophotometric methods were applied for determination of lactate and pyruvate. In the patients with recent cerebral infarction as compared with the control group an increase of glucose concentration was found in the blood (statistically significant) and in the CSF (statistically not significant), while the levels of lactate and pyruvate were raised in the CSF before as well as in the 8th and 16th minutes of the test. Absence of a statistically significant difference between lactate and pyruvate concentrations in the CSF in the same patients with recent cerebral infarction before and in the 8th and 16th minutes of the test suggests that glucose in a hypertonic solution failed to exert any significant influence on CSF lactate and pyruvate concentrations. These biochemical findings seem to support the observations of good therapeutic effects of glucose in hypertonic solution in some cases of cerebral infarction.

Adult↗
PubMedDate not supplied

[Traumatic cerebral infarct].

The clinical variants of traumatic cerebral infarction (TCI) were studied according to the results of computed tomography. It was found that TCI was encountered in 3.3% of patients with craniocerebral trauma. The localization and mechanism of the development of the ischemic lesion were determined by the character of the traumatic changes in the brain. Compression of the cerebral vessels and reduced perfusion pressure in intracranial three-dimensional processes are important in the pathogenesis of TCI. Computed tomographic studies must be repeated in order to establish the diagnosis of TCI.

Adult↗
PubMed1995

[Acute therapy and prevention of ischemic cerebral infarct].

The acute therapy of the cerebral infarct necessitates the fast evaluation of the favorable risk factors and the assessment of its pathogenetical mechanisms to facilitate a specific treatment as early as possible. Acute treatment procedures like the rheologic therapy, anticoagulation, thrombolysis, application of calcium antagonists, and antiedematous therapy are discussed. Recommendations for the secondary prophylaxis with drugs like acetylsalicylic acid or triclopidine after transitory ischemic attacks or manifest brain infarctions are given. The indications for the surgical therapy of stenoses of the extracranial vessels supplying the brain are discussed and rules for the emergency management of the transitory ischemic attack are introduced.

Brain Ischemia↗
PubMed1992

[Etiology and diagnosis of cerebral infarcts after the neonatal period].

QUESTION: After the neonatal period, cerebral infarctions are very rare in childhood. In the present study we aim to evaluate the etiology and diagnostic procedures of this disorder on the basis of our own experience. METHODS: We saw four children aged 3 2/12 to 11 4/12 years with a cerebral infarction at our hospital. Three children were followed up until 6 months after the infarction. The case reports are presented. On the background of the literature, the etiology and diagnostic possibilities and requirements are discussed. RESULTS: As the underlying cause, we saw a hemolytic-uremic syndrome in one case, and a (post-)infectious vasculitis following measles resp. scarlet fever in two cases. CCT, NMR, and transcranial Doppler sonography are the diagnostic methods of choice, although none of these by itself is able to diagnose this disorder with any certainty. Therapeutic measures are restricted to the causative disease. The prognosis is good quoad vitam, although serious regarding neurologic sequelae. CONCLUSIONS: An early diagnosis of this disorder is essential, because the only known effective therapy is the management of a possibly underlying disorder. Intensive physiotherapy as an additional measure is helpful to avoid neurological sequelae.

Cerebral Infarction↗
PubMed2003

Stroke subtype and mortality. a follow-up study in 998 patients with a first cerebral infarct.

The aim of this article was to study mortality following a first-ever cerebral infarct, accounting for ischemic stroke subtypes (lacunar, cardioembolic, atherothrombotic) and relevant prognostic variables. This study was done from s a hospital-based prospective registry of all patients with a first cerebral infarct, with a high case ascertainment of first and recurrent stroke by CT. We used a cross-sectional follow-up, using standardized methods. Analyses were performed using crude comparison of mortality data and death causes between stroke subtypes. We analyzed 30-day case fatality and 1-year mortality in 30-day survivors by means of logistic regression analysis, and mortality in 1-year survivors by means of Cox proportional hazard modeling. We also constructed Kaplan-Meier survival curves, and used log-rank testing for differences between stroke subtypes. Thirty-day case fatality was 10%, 1-year mortality 15%, and after 1-year mortality 16%. Mean follow-up was 691, SD 521 days. At the end of follow-up 36% of all patients had died. Mortality was at all three time points lowest in lacunar stroke (2, 12, and 14%, respectively), intermediate in atherothrombotic stroke (10, 16, and 15%, respectively), and highest in cardioembolic stroke (23, 22, and 21%, respectively). Death related to recurrent stroke was similar in all three stroke subtypes (13-16%). Although 30-day case fatality rate was low in lacunar stroke, a quarter of lacunar stroke patients had died at the end of follow-up. Diabetes mellitus, age, stroke subtype, and initial stroke severity were independent predictors of 30-day case fatality, but only diabetes and age were consistent independent predictors for later mortality. Recurrent stroke and heart failure were important death causes. Prognosis for (future) death following a first cerebral infarct differs between stroke subtypes; lacunar stroke patients have the lowest mortality. However, lacunar stroke cannot be regarded as a mild stroke type, as after 2 years more than a quarter of such stroke patients had died. Cardioembolic stroke patients have the grimmest prognosis: more than half of them had died within 1.5 years. Better prognosis for long-term survival following stroke may be achieved by therapies which lower the risk of stroke recurrence, provide better treatment of heart failure, or both.

Adult↗
PubMed1979

CT fogging effect with ischemic cerebral infarcts.

Systematic CT studies on ten patients with persistent ischemic cerebral infarct revealed a constant phenomenon, the fogging effect. The hypodense infarct at the beginning will be isodense, or close to isodense, on the plain CT during the seond of third weeks and at a later stage will be hypodense again. The fogging infarcted area shows homogeneous intensive contrast enhancement. Knowledge of the fogging effect is important for correct interpretation of the CT image and the indication for contrast medium CT. CT without contrast medium may lead to misinterpretation during the second and third weeks after the onset of cerebral infarction.

Brain Ischemia↗
PubMed1985

[Cerebral blood flow, cerebral oxygen metabolism, cerebral glucose metabolism, and tissue pH in human acute cerebral infarction using positron emission tomography].

It is necessary for treatment and deciding prognosis to make clear about changes of cerebral blood flow and metabolism in acute cerebral infarction. This preliminary PET study was designed to investigate physiological and biochemical changes in acute cerebral infarction by positron emission tomography (PET). PET studies were performed in six patients with acute cerebral infarction within 48 hours after onset of stroke using continuous inhalation of C15O2 for cerebral blood flow (CBF), 15O2 for cerebral metabolic rate for oxygen (CMRO2), 11CO for cerebral blood volume, the intravenous injection of 11C-dimethyloxazolidinedione for tissue pH and the intravenous injection of 18F-fluorodeoxyglucose for cerebral metabolic rate for glucose (CMRGlu). Metabolic coupling index (MCI) image was made from CBF image and CMRGlu image to investigate relation between CBF and CMRGlu. Also oxygen glucose index (OGI) image was made from CMRO2 image and CMRGlu image to investigate relation between CMRO2 and CMRGlu. Preliminary results demonstrate that reduction of CBF, CMRO2, and CMRGlu in the affected cortex except for reperfusion case. Increase of OER was recognized four of six cases. Patterns of MCI and OGI in the cortex which CMRO2 value is less than 65 mumol/100 g/min were different from those in the cortex which CMRO2 value is more than 65. MCI of the affected cortex (CMRO2 less than 65) decreased relative to that of the cortex (CMRO2 greater than or equal to 65). OGI of the affected cortex (CMRO2 less than 65) significantly decreased in comparison with that of the cortex (CMRO2 greater than or equal to 65).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Focal cerebral infarctions associated with perivascular tumor infiltrates in carcinomatous leptomeningeal metastases.

Diffuse carcinomatous leptomeningeal metastases "carcinomatous meningitis") have the usual clinical course involving multifocal nerve root deficits and a variable diffuse encephalopathy. In contrast, we describe a patient with carcinomatous leptomeningeal metastases who presented with clinical signs of meningitis and focal cerebral infarction. Over an 8-month period, multiple cerebral infarctions and cranial neuropathies developed. Postmortem examination of the patient's brain revealed diffuse leptomeningeal infiltration by a signet-ring adenocarcinoma. The extensive involvement of the subarachnoid space with tumor was associated with dense neoplastic infiltration of the Virchow-Robin spaces. These perivascular tumor infiltrates were accompanied by multifocal mural invasion and, less frequently, by intravascular tumor cells obliterating the lumen. Focal hemorrhagic infarcts in the cerebral cortex corresponded to areas of microscopic vasculopathy. This case provides evidence that tumor-associated vasculopathy with resultant ischemia plays a role in the pathogenesis of focal cerebral infarctions in carcinomatous leptomeningeal metastases.

Adenocarcinoma, Mucinous↗
PubMed2006

Diabetes is related to cerebral infarction but not to AD pathology in older persons.

OBJECTIVE: To examine the potential relation of diabetes to common neuropathologic causes of dementia, cerebral infarction and Alzheimer disease (AD) neuropathology. METHODS: Subjects were 233 older Catholic clergy in the Religious Orders Study, who underwent detailed annual evaluations, including neuropsychological testing, and brain autopsy at time of death (mean age 86 years, 45% men). Diabetes was identified by annual direct medication inspection and history. Cognitive function proximate to death was summarized into five cognitive domains, based on 19 neuropsychological tests. Macroscopic cerebral infarctions were recorded from 1 cm coronal slabs. Neuritic plaques, diffuse plaques, and neurofibrillary tangles were counted in Bielschowsky silver-stained sections and summarized to yield composite measures of neuritic plaques, diffuse plaques, tangles, and overall AD pathology. We also used immunohistochemistry with antibodies to amyloid-beta and PHF-tau to obtain quantitative measures of amyloid burden and neurofibrillary tangle density. Multiple logistic and linear regression analyses were used to examine the relation of diabetes to cerebral infarctions and AD pathology, controlling for age, sex, and education. RESULTS: AD pathology was related to all five cognitive domains (p < 0.01) and infarctions were related to perceptual speed (p < 0.001). Diabetes (present in 15% subjects) was associated with an increased odds of infarction (OR = 2.47, 95% CI: 1.16, 5.24). Diabetes was not related to global AD pathology score, or to specific measures of neuritic plaques, diffuse plaques or tangles, or to amyloid burden or tangle density. CONCLUSION: We found a relation between diabetes and cerebral infarction but not between diabetes and Alzheimer disease pathology in older persons.

Aged↗
PubMedDate not supplied

Cerebral infarction in a young female following snake bite.

We present a normal 13-year old female who developed left cerebral infarction following envenomation by the carpet viper (Echis carinatus). We have read of only one other case of cerebral infarction following viper envenomation (Viperi russelli). Possible mechanisms for cerebral infarction in these circumstances are discussed. It is believed that this complication may be more common than is reported in the literature.

Adolescent↗
PubMedDate not supplied

CT enhancement after prolonged high-dose contrast infusion in the early stage of cerebral infarction.

To demonstrate the BBB break-down on the CT image in the acute stage of cerebral infarction, a 3 hour continuous drip infusion of 200 ml of meglumine amidotrizoate, rather than the conventional bolus injection, was used. In this study, 22 examinations were carried out in 18 patients in whom cerebral infarction due to temporary or permanent obstruction of the cerebral artery was diagnosed by CT and angiography on admission. With each examination, the first CT was obtained prior to contrast infusion, and second immediately after the end of 3 hours of continuous contrast infusion. The EMI number was calculated at 3 regions of interest in the infarction. Within 3 days after stroke episode, 4 out of 5 patients with temporary vascular obstruction demonstrated enhancement, as well as 6 out of 9 patients with permanent vascular obstruction. Between 4 and 14 days after the stroke episode, all of 8 patients showed enhancement. To further clarify the extravasation of the contrast medium during the first 3 days of a cerebral infarction, a third CT scan was performed 3-hrs after finishing the contrast infusion in 4 patients. In these latter patients, blood was sampled at the time of each of the 3 CT series. The EMI number of the blood samples was also measured. In all 4 patients, the Gado's tissue-blood ratio (the EMI number of the CT lesion divided by that of the blood sample) was higher than 17.2% in the second, and higher than 54.7% in the third CT scan. Thus break-down of the BBB which was demonstrated by prolonged contrast infusion is an earlier event in human cerebral infarction than is usually accepted.

Blood-Brain Barrier↗