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PubMed1991

Parietal and bi-occipital lobe infarction confounded by ethanol-induced optic neuropathy.

A frequent occurrence in geriatric and chronically ill patients is the exhibition of several simultaneously occurring and confounding health problems. This paper reports the case of a 61-year-old-white male who presented with an extensive history of multiple brain infarcts, hemiparesis, personality changes and varied visual complaints. Tests in the neurooptometric work-up for this patient included static automated perimetry, stereoacuity and optokinetic nystagmus evaluation. The results were suggestive of multiple cerebrovascular accidents which included the right and left occipital lobes as well as the right parietal lobe. This clinical picture was complicated by the presence of nutritional or ethanol-induced optic neuropathy. Emphasis was placed on a detailed sequential history of events and a complete neurological and optometric evaluation to ascertain the multiple foci of cortical infarction. Corroboration of clinical findings was obtained by computerized axial tomography (CT scan).

Alcoholism↗
PubMed2003

[Common carotid artery intima-media thickness, carotid atherosclerosis and subtypes of ischemic cerebral disease].

INTRODUCTION: Common carotid artery intima-media thickness (CCA-IMT) measurements are widely used to study atherosclerosis. CCA-IMT is a useful outcome measure in clinical studies and intervention trials because it reflects early stages of atherosclerosis and cardiovascular risk. The present study examined the relationship between common carotid artery intima-media thickness and ischemic brain infarction. MATERIAL AND METHODS: The present study examined the association between CCA-IMT and incidence of ischemic stroke and its subtypes in 75 cases and 21 controls. Cases with internal borderzone infarction (IBI) were consecutively recruited and classified into subtypes using CT and Bamford's classification. It classifies cerebral infarctions regarding vascular territory using clinical features to determine the size and site of infarction. These subtypes included: total anterior circulation infarctions (TACIs), partial anterior circulation infarctions (PACIs), posterior circulation infarctions (POCIs), and lacunar infarctions (LACIs). Controls were recruited among individuals hospitalized at the same institution and matched for age and sex. Patients and control subjects underwent B-mode ultrasonographic measurements of IMT of the far wall of both common carotid arteries. RESULTS: Of 75 patients with acute ischemic stroke, 10 (14%) were classified as TACIs, 34 (45%) had PACIs, 12 (16%) had POCIs and 19 (25%) had LACIs. Mean CCA-IMT was higher in investigation group (1.03+/-0.18 mm) than in controls (0.85+/-0.18 mm; p<0.0001). The difference in CCA-IMT between investigation group and controls was significant and the relation between CCA-IMT and IBI remained unchanged after adjustments of main cardiovascular risk factors. Regarding the subtypes of IBI, IMT values were significantly higher in patients with TACIs and PACIs versus those with LACIs and POCIs. CONCLUSIONS: An increased CCA-IMT was established in all subtypes of IBI and was significantly higher in those with anterior circulation infarctions versus posterior circulation and lacunar infarctions. This study points to importance of noninvasive measurement of CCA-IMT with ultrasonographic techniques as a diagnostic tool for selecting patients at high risk for IBI and identifying different subtypes of ischemic stroke.

Arteriosclerosis↗
PubMed1986

[Locked-in syndrome in vascular pathology of the brain].

Seven patients with vascular abnormalities of the brain (infarct of the ventral portions of the pons varolii and/or the midbrain--5, hemorrhage into the base of the pons varolii--1 and transient impairment of the cerebral circulation in the vertebro-basilar system--presented the locked-in syndrome with such underlying disorders as tetraplegia with the maintenance of tendon and the appearance of abnormal plantar muscle reflexes, pseudobulbar syndrome with intact consciousness and the absence of any significant changes in the EEG. Other findings included disorders of eye movement, mainly in the horizontal plane and involuntary muscular activity such as forced crying, decerebrational and decorticational muscular spasms, as well as masticatory automatisms. The authors emphasize the identity of the given syndrome and Filimonov's syndrome which was repeatedly described in Soviet literature before 1966 when the term "locked-in syndrome" was proposed. They also discuss the pathogenetic mechanisms of the development of the locked-in syndrome in occlusion of the basilar artery.

Aged↗
PubMed2005

Pharmacological treatment of ischemic stroke.

Current pharmacological strategies for acute ischemic stroke largely mirror those employed in acute coronary syndromes. However, important differences in the effectiveness and versatility of the principal agents have emerged between these 2 clinical settings. In general, the level of success achieved with drugs in acute coronary syndromes has not carried over to the same extent when the same drug types are used in stroke. The principal reason is that reperfusion or anticoagulant therapies in the setting of brain infarction run a significant risk of hemorrhagic transformation that has no direct equivalent in myocardial infarction. Consequently, a significant challenge in acute stroke therapeutics is the ability to select patients for drugs where only a narrow therapeutic margin exists and to identify methods that can minimize hemorrhage risk. Other brain-specific vascular factors also pertain in explaining differences in outcome of drugs generally regarded as having a broad cardiovascular remit. The relatively limited efficacy of antiplatelets in stroke might relate to the composition and heterogeneity of the cerebrovascular lesion, while the poor outcome associated with acute anti-hypertensive use is partly due to loss of cerebrovascular autoregulation. Finally, downstream consequences of arterial occlusion within the brain such as excitotoxicity and plasticity are organ specific and, as such, deserve their own pharmacological approaches. In this review, we describe the general mechanism of each drug class used in ischemic stroke and then report on the clinical experience and application for each.

Animals↗
PubMed2003

Myocardial infarction and transient ventricular dysfunction in an adolescent with sickle cell disease.

We report a case of an adolescent who had sickle cell disease and previous evidence of myocardial damage and presented with abdominal pain and rapid progression to cardiogenic shock and subsequent development of myocardial infarction. To our knowledge, this represents only the second report of a case of acute myocardial ischemia and subsequent infarction resulting transient ventricular dysfunction reported in a child with sickle cell disease successfully treated with exchange transfusion. The pathophysiology of this complication remains unclear, and cardiac complications may remain undetected as lung, bone, and brain infarcts are more common and the pain associated with sickle cell crisis may mask the ischemic symptoms. Multiple factors may contribute to ischemia in addition to the presence of a vaso-occlusive crisis or infection. Acute or chronic myocardial ischemia are probably more prevalent than currently known.

Acute Disease↗
PubMed1992

[Status of cerebral and central hemodynamics in patients with ischemic stroke].

Overall 30 patients who suffered ischemic brain stroke were examined for cerebral and central hemodynamics by radiocerebrography (RC) with the aid of the radiopharmaceutical preparation Tx-99 and by radiocardiography (RCG) using 131I. These methods were employed simultaneously with computer-aided tomography, cerebral angiography, rheoencephalography. The control group was made up of 18 patients suffering from peripheral nervous diseases. In 11 patients with a favourable outcome of ischemic brain stroke and the recovery of work fitness, the RC and RCG readings did not practically differ from those in the controls. The remaining 19 patients with disability due to brain stroke demonstrated deceleration of the cerebral blood flow, most pronounced on the side of brain infarction. Asymmetry of the cerebral blood flow and deceleration of blood supply in the main and intracerebral vessels as shown by the RC readings turned out the signs of the hemodynamically significant stenosis of one of the internal carotid arteries, even in lack of the changes on the angiogram. A correlation was established between deterioration of central hemodynamics and deceleration of the cerebral blood flow, as was a possibility of an increase of the blood inflow to the brain after administering drugs that make the RCG readings return to normal.

Adult↗
PubMed2003

Neuronal expression of cell cycle-related proteins after brain ischaemia in man.

The death of neurons after brain ischaemia may be associated with activation of cyclin-dependent kinases (CDKs) and upregulation of cyclins, reflecting aberrant entry of neurons into the cell cycle. Little has been published on the expression of cell cycle proteins after brain ischaemia in man. Well-characterized antisera were therefore used to examine the neuronal expression of CDK2, CDK4 and cyclins A, D1 and E in sections of brain from patients who had experienced cardiac arrest or focal brain infarction, and died 3.5 h to 9 days later. Scattered neurons contained elevated levels of cyclin D1, CDK2 and, to a lesser extent, CDK4, but little or no cyclin A or E. Present findings indicate that brain ischaemia induces the entry of some neurons from G0 into the G1 phase of the cell cycle, and suggest a potential therapeutic role for CDK inhibitors in ischaemic stroke.

Adult↗
PubMed2003

Microsurgical intraluminal middle cerebral artery occlusion model in rodents.

OBJECTIVES: Focal brain ischemia induced in rodents by occlusion of the middle cerebral artery (MCA) is a widely used paradigm of human brain infarct. The objective of this study is to compare the effectiveness and reproducibility of MCA filament occlusion model in rats and mice. MATERIALS AND METHODS: A total of 140 rodents (69 rats and 71 mice) were operated. Ninety-five animals were subjected to MCA occlusion; the surgical procedure consisted of introducing an uncoated surgical nylon monofilament into the cervical common carotid artery (CCA) and advancing it intracranially to permanently block blood flow into the right MCA. Forty-five sham-occluded rodents underwent CCA ligation. Surgical success, autopsy confirmed success and mortality rate were evaluated. Effective MCA occlusion was confirmed by the evidence of motor neurological deficit, by histopathology, immunohistochemistry (IHC) and reverse transcriptase-polymerase chain reaction (RT-PCR). IHC was performed in a randomly selected number of animals to detect the protein product of monocyte chemoattractant protein-1. The brain tissue in mice was examined by RT-PCR for the expression of macrophage inflammatory protein-1 alpha mRNA. RESULTS: Surgical success rate was 89% in the rats, significantly lower than that in the mice (100%, P < 0.05). Autopsy confirmed success rate in the rats, 60%, was also significantly different from that in the mice (92.5%, P < 0.001). The operative mortality rate was 4.3% in the rats and 15% in the mice. CONCLUSION: The present study demonstrates that the microsurgical filament occlusion of the MCA can be more successfully performed in mice. The lower rate of success in rats seems to be as a result of the architecture of the carotid canal in this animal. No previous reports, using a considerable number of animals, have compared the feasibility of intraluminal model in the rat with that in the mouse.

Animals↗
PubMed1994

A double-blind study of neurotropin in patients with acute ischemic stroke.

Neurotropin was found to reduce brain oedema in an experimental model of brain infarction in the guinea-pig. A randomized double-blind controlled trial with Neurotropin was performed in 220 patients admitted within 24 h after an acute ischemic stroke. 35 of the neurotropin and 41 of the placebo-randomized patients had to be excluded. 10 included patients in the neurotropin and 13 in the placebo-treated group died within the study period of 15 days. A better clinical outcome was observed in the 65 included surviving neurotropin compared with the 56 placebo-treated patients. The size of the infarct and of the oedema zones was significantly more decreased on CT scans from Day 11 compared with Day 3 after stroke in the neurotropin than in the placebo treated group. Neurotropin is helpful in treating brain oedema, related to acute ischemic stroke.

Aged↗
PubMed1996

[Influence of social environments on brain aging].

To investigate influence of social activity on normal brain aging, we studied the social activity score, cognitive functions, self-rating depression scale, cerebral blood flow (CBF), MRI and motor function in the normal elderly people living in different social environments. There was no difference in risk factors for stroke, MRI findings and CBF between the two groups. However, the subjects living in a home for elderly showed significantly lower social activities than those living with families. Cognitive functions and motor function were lower, and SDS was higher in subjects living in retirement house than those living with families. The social environment including social activities closely related to life style may significantly influence brain aging with regard to silent brain infarctions or risk factors for stroke.

Aged↗
PubMed2001

[Detection of brain vascular diseases with CT angiography].

OBJECTIVE: To identify the diagnostic effect of spiral CT in brain vascular diseases. METHODS: Sixty four patients underwent CT angiography, including 22 patients with subarachnoid hemorrhage (SAH), 6 patients with oculomotor nerve paralysis, 5 patients with brain substance hemorrhage, 6 patients with arteriovenous malformation (AVM), 4 patients with mass or aneurysm, 5 patients with brain infarction, 16 patients with epilepsy or headache and dizzy. 8 cases also underwent digital subtraction angiography (DSA), 4 cases were performed operation in 64 cases. RESULTS: Spiral computed tomography angiography (SCTA) was all succeeded in 64 cases. 26 aneurysms and 8 AVMs were found by SCTA; in 6 of 8 cases of AVMs, their supply arteries and drainage veins were clearly displayed; SCTAs of 5 cases with substance hemorrhage were normal; in 1 of 5 cases with cerebral hemisphere infarction, its internal carotid obstruction was demonstrated by SCTA; the results of 12 SCTAs were identical with the results of their DSA or operation. CONCLUSION: SCTA is a useful non-invasive inspection method for detecting brain vascular diseases such as aneurysms and AVMs.

Adolescent↗
PubMed1995

Diffusion and perfusion MR imaging of cerebral ischemia.

Over the last few years, diffusion and perfusion magnetic resonance (MR) imaging methods have found increasing user for monitoring the effects of cerebral ischemia under clinical and experimental conditions. Blood perfusion can be visualized by studying the patency of the cerebrovascular bed (MR angiography), by recording exchange of diffusible tracers between blood and brain ([2H]water or [19F]trifluoromethane clearance), or by measuring the volume and transit time of the circulating blood (bolus track or spin-tagging imaging). In addition, changes in blood oxygenation level can be visualized by taking advantage of the susceptibility changes of the magnetic field homogeneity (functional or blood-oxygenation-level-dependent imaging). Diffusion imaging is based on the modulation of signal intensity by brain water diffusion. Recording a series of diffusion-weighted images allows calculation of the apparent diffusion coefficient (ADC) and the reconstruction of quantitative ADC images. Brain ADC changes are a function of intra-extracellular water homeostasis and therefore are a sensitive marker of ionic equilibrium. Since disturbances of ion and water homeostasis are among the first pathological alterations induced by brain ischemia, diffusion imaging is able to detect the incipient injury within minutes. Conversely, the reversal of these alterations is able to detect the incipient injury within minutes. Conversely, the reversal of these alterations is an early and reliable predictor of postischemic recovery. Applications of perfusion and diffusion imaging are reviewed in relation to the pathophysiology, the pathobiochemistry, and the therapy of evolving brain infarct after focal ischemia and the manifestation and reversal of ischemic injury during and after global ischemia.

Brain Ischemia↗
PubMed1996

[Pathology of the hemostatic system in the acute period of an ischemic stroke and the possibilities for its therapeutic correction].

The indices of blood haemostasis adequately reflecting the state of coagulative, fibrinolytic, anticoagulative and platelet aggregation systems were examined in 150 patients with acute ischemic stroke. The four haemostasiological syndromes such as hyperaggregation, hypercoagulation, depressed fibrinolysis, hypercoagulation and three types of thrombophilias were distinguished and described in detail. The special features of coagulopathic disorders depending on etiology, severity and stroke onset period were characterized. The authors developed some recommendations on selective medical correction of haemostatic disorders in acute period of brain infarction.

Acute Disease↗
PubMed1994

[Parma stroke data bank: atherothrombotic and lacunar stroke].

In an epidemiological research about stroke, we studied 235 patients with atherothrombotic brain infarctions and 81 patients with lacunes. It was a longitudinal study concerning patients admitted to our Medical Division during the acute phase and followed up for one year after the onset. We report some anamnestic data, the frequency of positive brain CT scan, main risk factors, symptoms at the onset, severity degree of the stroke within the first 72 hours, complications during, and outcome after, the first four weeks, including personal performances and environmental fitness, mortality rate and frequency of relapses. We also report some of these data after one year from the acute episode.

Adult↗
PubMed1998

Prediction of impending hemorrhagic transformation in ischemic stroke using magnetic resonance imaging in rats.

BACKGROUND AND PURPOSE: Hemorrhagic transformation (HT) of ischemic brain tissue may occur in stroke patients either spontaneously or after thrombolysis. A method to assess the risk of HT in ischemic tissue after stroke would improve the safety of thrombolytic therapy. As a means of predicting HT, we investigated the role of contrast-enhanced MRI at acute time points in a rat middle cerebral artery occlusion model with reperfusion. METHODS: Intraluminal suture occlusion of the middle cerebral artery was used to produce transient ischemia in male Wistar rats (n=11). Reperfusion was performed by withdrawal of the occluding filament after 2 (n=4), 3 (n=6), or 4 (n=1) hours. MRI studies were performed before and after reperfusion with the use of conventional T1-weighted imaging, with and without gadolinium (Gd-DTPA) contrast agent, and T2-weighted imaging. Follow-up MRI and histological studies were obtained at 24 hours. RESULTS: Petechial hemorrhage occurred by 24 hours in 9 of 11 animals. All animals showed brain swelling and cellular death throughout the ischemic region at 24 hours. A hyperintense region in the preoptic area became visible after Gd-DTPA injection within minutes after reperfusion in animals with subsequent HT. All animals showing acute Gd-DTPA enhancement subsequently developed petechial hemorrhage (or died) by 24 hours. In these animals, statistically significant differences in signal intensity (P=.0005) between the ipsilateral enhancing region and a homologous contralateral region were detected on post-Gd-DTPA T1-weighted imaging. There was also a statistically significant correlation (P=.01) between the rate of Gd-DTPA uptake and the size of the enhancing area. Two animals did not enhance with Gd-DTPA and did not exhibit hemorrhage on histological examination or MRI at 24 hours. No abnormalities were seen on precontrast T1-weighted images before and shortly after reperfusion or postcontrast T1-weighted images before reperfusion. CONCLUSIONS: The primary finding of this study was the detection of early Gd-DTPA parenchymal enhancement in 82% of the animals after reperfusion. Enhancement was seen before any detectable hemorrhage, suggesting that early endothelial ischemic damage occurs before gross brain infarction and hemorrhage. Thus, we suggest that acute Gd-DTPA enhancement may provide an early prediction of petechial hemorrhage.

Animals↗
PubMed2006

Antioxidant pyrrolidine dithiocarbamate activates Akt-GSK signaling and is neuroprotective in neonatal hypoxia-ischemia.

Pyrrolidine dithiocarbamate (PDTC), an antioxidant and inhibitor of transcription factor nuclear factor kappa-B (NF-kappaB), has been reported to reduce inflammation and apoptosis. Because PDTC was recently found to protect in various models of adult brain ischemia with a wide therapeutic time window, we tested the effect of PDTC in a rodent model of neonatal hypoxia-ischemia (HI) brain injury. T2-weighed magnetic resonance imaging (T2-MRI) 7 days after the insult showed that a single PDTC (50 mg/kg) injection 2.5 h after the HI reduced the mean brain infarct size by 59%. PDTC reduced the HI-induced dephosphorylation of Akt and glycogen synthase kinase-3beta (GSK-3beta), expression of cleaved caspase-3, and nuclear translocation of NF-kappaB in the neonatal brain. PDTC targeted directly neurons, as PDTC reduced hypoxia-reoxygenation-induced cell death in pure hippocampal neuronal cultures. It is suggested that in addition to the previously indicated NF-kappaB inhibition as a protective mechanism of PDTC treatment, PDTC may reduce HI-induced brain injury at least partially by acting as an antioxidant, which reduces the Akt-GSK-3beta pathway of apoptotic cell death. The clinically approved PDTC and its analogues may be beneficial after HI insults with a reasonable time window.

Animals↗
PubMed1999

Cerebral tomographic findings in patients undergoing carotid endarterectomy for asymptomatic carotid stenosis: short-term and long-term implications.

PURPOSE: Preoperative cerebral imaging has been considered not to be cost-effective in carotid endarterectomy (CEA) for asymptomatic carotid stenosis. Yet, silent brain infarction (SBI) has been associated with the embolization potential of a severe carotid stenosis. Thus the presence of SBI may represent an additional indication for CEA in asymptomatic patients. We examined the predictive value of preoperatively detected silent cerebral lesions on early and late outcomes in patients undergoing CEA for asymptomatic carotid stenosis. METHODS: Preoperative cerebral tomographic (CT) scans performed on 301 asymptomatic patients undergoing 346 CEAs from 1986 to 1995 were reviewed by a single neuroradiologist blinded to patients' records. Mean follow-up was 67. 3 months (range, 24-130 months). The degree of internal carotid lumen reduction was measured bilaterally in all patients (602 carotid arteries); carotid stenosis of 60% or more was found in 399 carotid arteries. RESULTS: Of the 103 (34%) CT scans positive for cerebral lesions, 58% were lacunar. No significant association was observed between the side of the cerebral lesion on CT scan and the severity of the corresponding carotid stenosis; 38 silent lesions were detected in the 203 hemispheres ipsilateral to carotid stenoses that were less than 60% versus 95 SBIs in the 399 hemispheres ipsilateral to carotid stenoses that were 60% or more (19% vs 24%; P =.2). There were no significant differences in the perioperative stroke/death rate in patients with or without cerebral CT lesions (2% vs 1%; odds ratio, 1.94; P =.6). Mortality rate during follow-up was 22% in patients with preoperative SBI and 15% in patients without SBI (P =.1). However, actuarial survival at 10 years was shorter (P =.02) in patients with SBI. Late stroke occurred in 11% of patients with preoperative SBI and in 3% of patients without preoperative SBI (P =.006). Cox regression analysis showed that both preoperative lacunar and nonlacunar infarctions were independent predictors of late stroke (hazard ratio, 3.6; P =.04; and hazard ratio, 7.1; P =.001; respectively). CONCLUSION: In our experience, preoperative SBI did not occur more frequently in the hemisphere ipsilateral to asymptomatic severe carotid stenosis. Although our study lacks a medically treated control group, our data show that SBI is predictive of poor neurologic outcome in asymptomatic patients undergoing CEA. We conclude that CT before CEA, selectively applied, provides information on long-term neurologic prognosis and that a less aggressive attitude towards CEA in asymptomatic patients with SBI may be justified.

Adult↗
PubMed2005

A matrix metalloproteinase protein array reveals a strong relation between MMP-9 and MMP-13 with diffusion-weighted image lesion increase in human stroke.

BACKGROUND AND PURPOSE: Matrix metalloproteinases (MMPs) are involved in tissue destruction produced by the neuroinflammatory response that follows ischemic stroke. In the present study we use an MMP array to investigate the blood levels of several MMPs in stroke patients and its relation with brain tissue damage and neurological outcome. METHODS: Twenty-four patients with middle cerebral artery occlusion who received thrombolytic therapy were included. Blood samples were drawn before tissue plasminogen activator treatment and an MMP array (multiplex enzyme-linked immunosorbent assay [ELISA]) was performed including gelatinases (MMP-2 and MMP-9), collagenases (MMP-1, MMP-8, and MMP-13), stromelysines (MMP-3 and MMP-10), and MMP endogen inhibitors (TIMP-1 and TIMP-2). To assess tissue lesion a serial multimodal MRI study was performed (pretreatment and at 24 hours). RESULTS: Neither initial diffusion lesion nor hypoperfused volume was associated with metalloproteinase expression within the first 3 hours after stroke onset. Nevertheless, a strong correlation was found between MMP-9 and MMP-13 with diffusion-weighted image (DWI) lesion expansion (r=0.54, P=0.05 and r=0.60, P=0.017, respectively). Baseline levels of both MMP-9 (OR, 14;95% CI, 1.5 to 131; P=0.019) and MMP-13 (OR, 73; 95% CI, 3.9 to 1388; P=0.004) were independent predictors of final increase in brain infarct volume at 24 hours. CONCLUSIONS: Our results demonstrate that within the neuroinflammatory response, high levels of MMP-9 and MMP-13 are involved in DWI lesion growth despite thrombolytic therapy, suggesting its ultra-early role in brain injury.

Aged↗