[Frequency of cerebral infarction with patent cerebral arteries].
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Cerebrovascular Disorders↗
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Experimental study on the effect of antegrade cerebral perfusion on brains with old cerebral infarction.
OBJECTIVE: Patients with old cerebral infarction who undergo aortic arch operations are susceptible to postoperative neurologic dysfunction. To verify such susceptibility, we performed this experimental study. METHODS: A cerebral infarct model was created in mongrel dogs by means of injection of cylindrical silicone embolus through the internal carotid artery. The dogs that had obvious neurologic deficits 1 day later and survived for 4 weeks or more were included in the cerebral infarct model. One month after cerebral infarction was induced, deep hypothermia and selective cerebral perfusion were used in 14 mongrel dogs (infarct group, n = 7; control group, n = 7). During this procedure, serum glutamate concentration and venous-arterial lactate difference were measured. Histopathologic study of the brain was also performed. RESULTS: Changes in venous-arterial lactate difference in both groups were almost similar, except in the rewarming phase. At 32 degrees C during rewarming, the venous-arterial lactate difference in the infarct group was significantly higher than that in the control group (P =.006). Although pre-cooling concentrations of serum glutamate were similar in both groups, the values in the infarct group at the end of rewarming were significantly higher than those in the control group (P =.046). On histologic examination, the presence of old cerebral infarction with gliosis was confirmed in the infarct group, but neither new cerebral infarction nor destruction of the blood-brain barrier was found. CONCLUSION: We observed an accelerated anaerobic metabolism and an increased extracellular glutamate release in the infarct group. The brain with old cerebral infarction is more susceptible to ischemia during arch operation than noninfarcted brain.
Animals↗
Human C-reactive protein increases cerebral infarct size after middle cerebral artery occlusion in adult rats.
Human C-reactive protein (CRP), the classic acute phase plasma protein, increases in concentration after myocardial infarction and stroke. Human CRP binds to ligands exposed in damaged tissue and can then activate complement and its proinflammatory functions. In contrast, rat CRP, which binds to similar ligands, does not activate complement. In the present study, systemic complement depletion with cobra venom factor in adult rats subjected to middle cerebral artery occlusion did not affect cerebral infarct size, indicating that circulating complement does not contribute to injury in this model. However, we have previously reported that administration of human CRP to rats undergoing coronary artery ligation caused a marked increase in size of the resulting myocardial infarction, associated with codeposition of human CRP and rat complement in the infarcts. In the present study, we show that adult rats subjected to middle cerebral artery occlusion and then treated with human CRP similarly developed significantly larger cerebral infarcts compared with control subjects receiving human serum albumin. Human CRP can thus contribute to ischemic tissue damage in the brain as well as in the heart, and inhibition of CRP binding may therefore be a promising target for tissue protective acute therapeutic intervention in stroke as well as in myocardial infarction.
Aging↗
Multiple cerebral infarctions from nonbacterial thrombotic endocarditis mimicking cerebral vasculitis.
Primary vasculitis of the central nervous system (PVCNS) is an uncommon disorder that can present with a variety of symptoms, making diagnosis and management difficult. We describe a case of cerebral infarction that occurred from nonbacterial thrombotic endocarditis (NBTE) and presented with clinical and radiologic imaging features that suggested PVCNS. The patient was a 58-year-old woman with left hemiparesis, aphasia, and episodic confusion. Magnetic resonance imaging of the brain demonstrated multifocal lesions consistent with infarction involving both cerebral hemispheres, and cerebral angiography showed changes consistent with vasculitis. Although brain biopsy findings were normal, the patient was treated for presumed vasculitis with cyclophosphamide and prednisone. Four months later respiratory failure secondary to polymicrobial pneumonia and adult respiratory distress syndrome developed, and she died. Autopsy revealed multiple infarcts in the heart, lungs, right kidney, spleen, and brain. Multiple thrombotic platelet-fibrin vegetations consistent with NBTE were found on all cardiac valves. Examination of the brain revealed no evidence of active or healed vasculitis. Cerebral angiography may show findings that suggest vasculitis, but it is not diagnostic, as several other conditions may cause similar changes. Nonbacterial thrombotic endocarditis may cause multiple cerebral infarctions and can be difficult to distinguish from vasculitis, as specific diagnostic tests for PVCNS are lacking.
Autopsy↗
Reversible vascular changes in children with cerebral infarction.
A case of cerebral infarction in a 4-year-old male is described. The child presented with an acute onset of right hemiplegia, central facial palsy, and dysarthria. He had no predisposing factors for cerebral infarction. A computed tomography scan showed a diffuse low-density area in the territory of the left miiddle cerebral artery. Magnetic resonance angiography disclosed multiple irregular narrowings in the left anterior and middle cerebral arteries. He recovered spontaneously from the stroke with minimal long-term complications, and repeated angiography disclosed a complete regression of the vascular changes 2 months after the stroke. There was no recurrence of stroke after 2-year follow-up. This case demonstrates the importance of longitudinal angiographic follow-up in childhood cerebral infarction of idiopathic origin.
Child↗
[Early diagnosis of cerebral infarct. Hyperdensity of the middle cerebral artery as the first CT sign of an ischemic lesion].
An early CT sign of cerebral infarction in the sylvian area is described: the normal density value of the middle homolateral cerebral artery is increased, because of thrombotic or embolic deposits inside.
Adult↗
Mechanisms of acute cerebral infarctions in patients with middle cerebral artery stenosis: a diffusion-weighted imaging and microemboli monitoring study.
Although most therapeutic efforts and experimental stroke models focus on the concept of complete occlusion of the middle cerebral artery as a result of embolism from the carotid artery or cardiac chamber, relatively little is known about the stroke mechanism of intrinsic middle cerebral artery stenosis. Differences in stroke pathophysiology may require different strategies for prevention and treatment. We prospectively studied 30 consecutive acute ischemic stroke patients with middle cerebral artery stenosis detected by transcranial Doppler and magnetic resonance angiography. Patients underwent microembolic signal monitoring by transcranial Doppler and diffusion-weighted magnetic resonance imaging. Characteristics of acute infarct on diffusion-weighted magnetic resonance imaging were categorized according to the number (single or multiple infarcts) and the pattern of cerebral infarcts (cortical, border zone, or perforating artery territory infarcts). The data of microembolic signals and diffusion-weighted magnetic resonance imaging were assessed blindly and independently by separate observers. Diffusion-weighted magnetic resonance imaging showed that 15 patients (50%) had single acute cerebral infarcts and 15 patients had multiple acute cerebral infarcts. Among patients with multiple acute infarcts, unilateral, deep, chainlike border zone infarcts were the most common pattern (11 patients, 73%), and for single infarcts, penetrating artery infarcts were the most common (10 patients, 67%). Microembolic signals were detected in 10 patients (33%). The median number of microembolic signals per 30 minutes was 15 (range, 3-102). Microembolic signals were found in 9 patients with multiple infarcts and in 1 patient with a single infarct (p = 0.002, chi(2)). The number of microembolic signals predicted the number of acute infarcts on diffusion-weighted magnetic resonance imaging (linear regression, adjusted R(2) =0.475, p < 0.001). Common stroke mechanisms in patients with middle cerebral artery stenosis are the occlusion of a single penetrating artery to produce a small subcortical lacuna-like infarct and an artery-to-artery embolism with impaired clearance of emboli that produces multiple small cerebral infarcts, especially along the border zone region.
Acute Disease↗
[An infantile case of cerebral infarction associated with thrombocytosis].
Cerebral infarction in children is often caused by intracranial vascular disorder, cardiac disease, head injury, or infection, and is rarely induced by blood disease. In this paper, we describe an infantile case of cerebral infarction associated with thrombocytosis. A female infant of eight months of age developed left hemiparesis after a slight head injury. Her CT and MRI demonstrated a cerebral infarction located from the right internal capsule to the right corona radiata. Laboratory findings revealed iron-deficiency anemia and thrombocytosis with a platelet count 107.5 x 10(4)/mm3. Although she had no disorder that had caused iron deficiency, serum Fe value of the patient was low with a count of 18 micrograms/dl. Her bone marrow was normal except for a slight increase in the number of megakaryocytes. One month later, her anemia was improved by means of oral iron replacement. However, her platelet count remained at more than 100 x 10(4)/mm3 as it had been before. Her condition of left-sided hemiparesis gradually improved by a program of rehabilitation, and did not recur after aspirin administration. Although the main cause of her thrombocytosis that led to a transient cerebrovascular accident is obscure, it is postulated that her iron deficiency anemia induced secondary thrombocytosis, or else the patient had essential thrombocytosis.
Anemia, Hypochromic↗
Time course of cerebral infarction in the middle cerebral arterial territory: deep watershed versus territorial subtypes on diffusion-weighted MR images.
PURPOSE: To examine possible differences between the evolution of cerebral watershed infarction (WI) and that of territorial thromboembolic infarction (TI) by using diffusion-weighted (DW) and T2-weighted magnetic resonance (MR) images and apparent diffusion coefficient (ADC) maps. MATERIALS AND METHODS: Fourteen patients with TI and nine with WI underwent MR imaging from the acute to chronic infarction stages. ADC maps were derived from DW images. Lesion-to-normal tissue signal intensity ratios on ADC maps (rADC), echo-planar T2-weighted images, and DW images were calculated. Lesion volumes at acute or early subacute infarction stages were measured on DW images, and final lesion volumes were estimated on fluid-attenuated inversion-recovery images. RESULTS: Analysis of variance revealed a significant difference in temporal evolution patterns of rADC between WI and TI (P <.001). rADC pseudonormalization following TI began about 10 days after symptom onset, but that following WI did not occur until about 1 month after symptom onset. The Pearson correlation coefficient between final and initial infarct volumes was 0.9899 for both infarction subtypes, indicating that the initial ischemic injury volume measured at the acute or early subacute stage predicted the final lesion volume fairly well. CONCLUSION: The evolution time of ADC is faster for TI than for WI. This difference, which likely originates from the different pathophysiologic and hemodynamic features of the two infarction types, might account for the relatively large range of ADC values reported for the time course of ischemic strokes.
Acute Disease↗
Cerebral infarcts in full term neonates.
Cerebral infarcts are an important cause of neonatal convulsions. We report the etiologic factors, and clinical and neuroradiologic findings of four full term neonates who presented with neonatal convulsions and had cerebral infarct. In our patients the risk factors for the cerebral infarct were perinatal asphyxia, sepsis, dehydration and catheter application. All had convulsions as the initial sign of infarct and had cranial imaging which revealed the definitive diagnosis. The patients underwent an extensive evaluation for hereditary causes of cerebral infarct that included anticoagulant factors (Proteins C and S, antithrombin III, antiphospholipid antibodies), factor V Leiden and prothrombin gene mutations, blood and urine amino acid and urine organic acid levels. The results were found to be within normal limits. In conclusion, neonatal convulsions can be the first sign of cerebral infarct. For this reason it seems preferable to include cranial imaging by computed tomography or magnetic resonance imaging (MRI) in the work-up of cases with unexplained neonatal convulsions.
Cerebral Infarction↗
Beagle puppy model of perinatal cerebral infarction. Acute changes in regional cerebral prostaglandins during hemorrhagic hypotension.
Perinatal cerebral infarction is a not uncommon finding in newborn babies surviving intensive care. Asphyxia, with its attendant hypotension, is the most common cause of this problem and may result in neuropathological changes in the periventricular white matter. Previous studies have demonstrated uncoupling of cerebral blood flow and metabolism in the periventricular white matter regions of newborn beagle pups exposed to hemorrhagic hypotension. This work examines the effects of hypotension on serum and regional cerebral prostaglandin levels in the newborn beagle pup. The animals were anesthetized, tracheostomized, and paralyzed. Pups were randomly assigned to two groups: one was subjected to hemorrhagic hypotension and the other received no insult. Hypotension was induced by slow venous hemorrhage calculated to maintain a mean arterial blood pressure at 20 to 30 mm Hg. Serum prostaglandin determinations were made immediately before and 15 minutes after random assignment to hypotension or control groups. In addition, regional cerebral prostaglandin determinations were performed 15 minutes after randomization. Analysis of the serum prostaglandin data revealed that there were no significant differences in the values for thromboxane B2 or 6-keto-prostaglandin (PG) F1 alpha, which are the stable breakdown products of thromboxane A2 and prostacyclin, respectively. Prostaglandin E2 levels increased in response to hemorrhagic hypotension insult. Regional cerebral prostaglandin determinations demonstrated decreases in thromboxane B2 and 6-keto-PGF1 alpha in both gray and white matter. Although gray matter PGE2 was increased in pups exposed to hemorrhagic hypotension, this increase was not found in the periventricular white matter of injured pups. This regional difference in PGE2 synthesis in response to insult may explain the periventricular white matter neuropathological changes attributed to it.
Animals↗
Cerebral infarcts related to isolated middle cerebral artery stenosis.
BACKGROUND AND PURPOSE: The clinical presentation of middle cerebral artery (MCA) stenosis, a rarely diagnosed condition, is not well known. The aim of this study was to analyze the stroke patterns of patients with isolated MCA stenosis. METHODS: Twenty-two patients with cerebral infarcts due to isolated MCA stenosis were analyzed with respect to their clinical syndrome, and cerebral lesions were assessed by neuroimaging. MCA stenosis was diagnosed by transcranial Doppler sonography (TCD) in 16, by TCD and digital subtraction angiography (DSA) in 4, and by DSA alone in 2 patients. RESULTS: Ten patients (45.5%) had lacunar syndromes, suggesting small-vessel disease, and 12 patients (55.5%) showed signs and symptoms of cortical dysfunction. Cerebral CT or MRI showed no lesion in 2 patients, small deep infarcts in 10, large striatocapsular infarcts in 2, combined piomedullary and striatocapsular infarcts in 4, piomedullary branch infarcts in 3, and MCA trunk infarct in 1. CONCLUSIONS: The results suggest an association between MCA stenosis and (1) lacunar infarcts and (2) the occurrence of piomedullary MCA branch infarcts alone or in combination with subcortical infarcts. The clinical syndromes and the radiological findings correspond in most cases.
Adult↗
[Clinical assessment of cerebral infarction, complicated with aortic arch replacement under selective cerebral perfusion].
Since October 1984 to December 1992, 47 aortic arch replacements were performed under selective cerebral perfusion (SCP). Patient age ranged from 19 to 81 years, with an average of 60.2 years. Thirty one patients were male and 16 female. Twenty patients were diagnosed with dissecting aneurysms, 27 true aneurysms. The operative mortality was 14 out of 47 (29.8%) over all. The mortality of dissecting aneurysm related acuity that is 5 of 9 (55.6%) for patients in acute phase, against none in chronic. The operative mortality of true aneurysms was 6 out of 11 (54.5%) for patients who had emergency operation, against 3 out of 16 (18.8%) scheduled, extensive surgery. Cerebral disorders developed on 8 patients out of 44 (18.2%, except 3 operative deaths). The mortality rate of cerebral disorder was 6 out of 8 (75.0%). Six patients with true aneurysm had cerebral infarctions after the surgery. Two patients had already cerebral disorders in advance the surgery. The cause of cerebral infarction was resumed by atherosclerotic materials. Our operative results indicate that cerebral disorder subsequently affects the mortality of aortic arch replacement. For the prevention of cerebral infarction, we modified the method of SCP. We start the SCP at the initiation of total cardiopulmonary bypass, routinely associated to an aortic clamp and cardiac arrest under myocardial protective procedure that is the use of perfusion cooling (30 degrees C, monitored at the esophagus), topical cooling and cold Saint Thomas solution infused in the coronary arteries. When aortic arch replacement is done, we need to make sure a good restarting of the heart and a good recovery of the systemic circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Unexpected accumulation of thallium-201 in cerebral infarction.
Three cases of cerebral infarct that unexpectedly showed accumulation of thallium-201 on single photon emission CT are presented here. In the first case, infarction developed following removal of an intracerebral hematoma. In the second case, infarction developed due to deep venous thrombosis as demonstrated by angiography. In the third case, hemorrhagic infarction was diagnosed by the follow-up CT. The findings in these cases demonstrate that thallium-201 accumulation may occur in the liquefaction stage of cerebral infarction.
Aged↗
Delayed decompressive surgery increases apparent diffusion coefficient and improves peri-infarct perfusion in rats with space-occupying cerebral infarction.
BACKGROUND AND PURPOSE: There is no conclusive experimental support that decompressive surgery in late stages of space-occupying cerebral infarction will improve outcome. We studied the effects of delayed decompressive surgery on the development of tissue damage, edema formation, and cerebral perfusion with different MRI techniques in a rat model of space-occupying cerebral infarction. METHODS: Permanent middle cerebral artery (MCA) occlusion was performed in 6 Fisher 344 rats. Decompressive surgery was performed 17 hours after the occlusion. Each animal was assessed before surgery and 2 and 4 hours after surgery by means, of diffusion-weighted T2-weighted, and flow-sensitive alternating inversion recovery perfusion-weighted MRI. Ischemic damage was also evaluated in hematoxylin-eosin-stained brain sections. RESULTS: Lesion volume as derived from apparent diffusion coefficient (ADC) maps decreased from 522+/-98 mm3 before to 405+/-100 mm3 (P=0.016) 4 hours after decompressive surgery, whereas lesion volume from T2 maps increased from 420+/-66 mm3 before to 510+/-92 mm3 (P=0.048) 4 hours after decompressive surgery. Midline shift decreased from 1.4+/-0.1 mm to 0.5+/-0.2 mm (P=0.001). Blood flow in the noninfarcted area of the ipsilateral hemisphere improved from 25+/-9 mL/min/100 g of tissue to 38+/-9 mL/min/100 g of tissue (P=0.035). Despite the pseudonormalization of ADC, irreversible damage was found in the entire MCA territory on histological evaluation. CONCLUSIONS: In rats with space-occupying cerebral infarction, delayed decompressive surgery leads to a decrease in lesion volume derived from ADC maps, which is probably because of an increase of extracellular water formation. There are no signs that this reflects rescue of ischemic tissue.
Animals↗
[Cerebral blood flow increase and P300 latency prolongation by intravenous injection of acetazolamide--investigation in lacunar cerebral infarction and healthy subjects].
The cerebral blood flow and the P300 were measured before and 20 minutes after intravenous injection of 17 mg/kg acetazolamide in 15 cases of lacunar cerebral infarction and 10 healthy subjects. In cerebral infarction, the study was performed within 2 weeks after the onset. The cerebral blood flow except the infarcted area was increased significantly by the intravenous injection of acetazolamide in the lacunar cerebral infarction group and the healthy subject group. The blood flow decrease around the infarcted area (intracerebral steal phenomenon) by the intravenous injection of acetazolamide was not observed in any case. The N200 latency and the P300 latency were prolonged significantly by the intravenous injection of acetazolamide in the lacunar cerebral infarction group and in the healthy subject group but the N100 latency and the P200 latency did not show any significant changes. Despite the increase in cerebral blood flow, cerebral function may be decreased by intravenous injection of acetazolamide.
Acetazolamide↗
Extensive cerebral infarction due to involvement of both anterior cerebral arteries by Wegener's granulomatosis.
The central nervous system is often affected in Wegener's granulomatosis (WG), but massive cerebral infarction due to occlusion of branches of the anterior cerebral arteries (ACA) by granulomatous lesions or thrombosis, or both, has seldom been reported. A case is reported here of a 67 year old man with WG complicated by generalised necrotising vasculitis in the lung, kidney, and gastrointestinal tract, and cerebral infarction in the territory of both anterior cerebral arteries, probably caused by thrombosis and a contiguous invasion of granulomatous lesion from the nasal cavity.
Aged↗
Perinatal cerebral infarction.
The diagnosis of perinatal cerebral infarction, although frequently suggested clinically, has been made most commonly at postmortem examination; few infants surviving stroke are reported in the literature. We evaluated 18 infants with perinatal cerebral infarction in a recent twelve-month interval. Seven were preterm neonates, 6 of whom had experienced neonatal intraventricular hemorrhage. Three full-term infants were thought to have experienced cerebral infarction in utero and had evidence of well-defined strokes on computed tomographic scans performed shortly after birth. Eight infants developed stroke at term. The most common cause of cerebral infarction in our series was perinatal asphyxia. Fourteen of the infants were seen with neonatal seizures. Fourteen of the 18 have died or are faring poorly at 4 to 12 months of age (corrected).
Asphyxia Neonatorum↗