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Magnetization transfer, HASTE, and FLAIR imaging.

Continuous technologic developments and research have increased the clinical applications of MT, HASTE, and FLAIR imaging in neuroradiology. HASTE has become the MR imaging sequence of choice for fetal neuroimaging. Other promising uses, such as for diffusion-weighted imaging, have not been fully exploited. FLAIR has been firmly established as one of the cornerstones of brain imaging; however, post-contrast FLAIR images have not offered a clear advantage over standard T1-weighted images as suggested by early studies. FLAIR imaging with echoplanar acquisition is not considered advantageous, because the decreased imaging times are obtained at the expense of lower sensitivity. For a number of applications, diffusion-weighted imaging has surpassed FLAIR. Nevertheless, FLAIR images may be more sensitive for the detection of acute brain infarction. Recently described methods for the elimination of CSF flow artifacts may lead to improved quality and reliability of FLAIR images for subarachnoid space disease. MT preparation is now routinely incorporated in time-of-flight MR angiography and gradient-echo T2*-weighted spine imaging sequences and provides increased sensitivity for postcontrast MR imaging. These applications may not be advantageous in all clinical settings. MTR analysis offers valuable information for an increasing number of pathologic processes but has not yet gained wide clinical acceptance owing to sophisticated postprocessing and significant intercenter variations. Different modifications of these techniques are being evaluated, and further developments are expected.

Brain↗

Characterization of the cerebroprotective efficacy of the competitive NMDA receptor antagonist CGP40116 in a rat model of focal cerebral ischemia: an in vivo magnetic resonance imaging study.

The cerebroprotective properties of the competitive NMDA antagonist D-(E)-2-amino-4-methyl-5-phosphono-3-pentenoic acid (CGP 40116) were evaluated in a rat model of focal cerebral ischemia. CGP 40116 (5-40 mg/kg i.v.) was injected immediately following permanent occlusion of the left middle cerebral artery (MCA). MK 801 (1 or 3 mg/kg i.v.), D-CPPene (20 mg/kg i.v.), and CGS 19755 (40 mg/kg i.v.) were used for comparison. Lesion volume was assessed using in vivo magnetic resonance imaging, which in initial experiments with parallel histological determinations proved to be an accurate method for the measurement of brain infarction and the determination of a cerebroprotective drug effect. CGP 40116 dose-dependently reduced the volume of cortical infarction, with an ED50 of 11 mg/kg i.v. and a maximal effect equivalent to a 62% reduction in cortical edema volume. Its cerebroprotective efficacy was thus comparable to that of MK 801. The rank order of potency for the NMDA antagonists was MK 801 > CGP 40116 approximately D-CPPene > CGS 19755. Neuroprotection by CGP 40116 was still apparent when treatment was started 30 min after MCA occlusion. It is concluded that CGP 40116 is an effective cerebroprotectant with potential clinical utility for amelioration of focal cerebral ischemic damage.

2-Amino-5-phosphonovalerate↗

Recurrent stroke and vascular events in elderly patients with anticardiolipin antibodies: a prospective study.

The presence of anticardiolipin antibodies (aCL) is a recognized risk factor for ischaemic stroke and a predictor of recurrent ischaemic events in young patients, but the significance of positive aCL tests is uncertain in the elderly. We evaluated the frequency of aCL and the risk of recurrence of stroke and other vascular events in a series of 242 consecutive patients aged over 60 years, admitted for brain infarction. All underwent aCL immunoreactivity (ELISA; measured by IgG antiphospholipid, GPL, units) and transoesophageal echocardiography and were later examined or contacted by telephone (mean 2.33 +/- 1.25 years, max. 4). Fifty patients (21 %) had at least l0 GPL units aCL. There were no differences between these and the other patients in the results of transoesophageal echocardiography, including mitral or aortic valvular thickening, atrial thrombus, atrial spontaneous contrast, strands, and aortic plaques thickness. None had IgG higher than 80 GPL units or was positive for anti-beta2 glycoprotein I. Patients with at least 10 GPL units more often had a past history of cerebral infarction than patients lower aCL level. However, the incidence of recurrent stroke was 4.5 per 100 person-year in patients with more than 10 GPL units, and 2.7 per 100 person-year in those with more than 10 GPL units. Kaplan-Meier analysis for any vascular events showed no differences between the two groups. In contrast to young patients, elderly patients with 10 or more GPL units aCL and negative for anti-beta2 glycoprotein I do not seem to have a higher risk of vascular events.

Aged↗

[Antiplatelet drugs for prevention of cerebral ischemic accidents].

Antiplatelet (AP) drugs play a major role in stroke prevention. Aspirin (50-1300 mg), ticlopidine (500 mg), clopidogrel (75 mg) and dipyridamole (400 mg) are effective in secondary prevention of atherothrombotic brain infarcts. Aspirin has been the most extensively studied drug and remains the most cost-effective one. The optimal dose is still debated; doses between 100 and 300 mg are the most widely used. The preventive efficacy of aspirin is already present at the acute phase of cerebral infarct. In primary prevention, aspirin nearly halves the risk of myocardial infarction but does not reduce that of stroke. Cardiac diseases with a high embolic risk require the use of oral anticoagulation. In non valvular atrial fibrillation, the choice of antithrombotic drugs depends on risk stratification: oral anticoagulants are indicated in high risk subjects whereas aspirin is recommended in low risk subjects and when oral anticoagulants are contraindicated. Studies with new associations of AP and with new drugs are required to increase the yield of the antiplatelet approach in high risk subjects; this should be done in parallel with efforts to detect and to treat the vascular risk factors associated with the development of a mass approach for stroke primary prevention.

Brain Ischemia↗

A multicentre, double-blind, randomized study to compare the safety and efficacy of once-daily ORG 10172 and twice-daily low-dose heparin in preventing deep-vein thrombosis in patients with acute ischaemic stroke.

A multicentre, double-blind, randomized study was performed in 179 patients with acute ischaemic stroke resulting in limb paresis. The purpose was to compare the safety and efficacy of Org 10172 (1250 anti-Xa Units s.c. once daily) and heparin sodium (5000 IU s.c. twice daily) in preventing deep-vein thrombosis (DVT). Prophylaxis started within 72 hours of the onset of stroke and continued for at least 9 days. To detect DVT, patients underwent a daily 125I-fibrinogen leg scanning which, if found positive, was followed by venography. A first computed tomography scan of the brain was performed at screening to rule out cerebral haemorrhage and a second at cessation of treatment to detect any haemorrhagic transformations. At the 2-3-months' follow-up period the patients were examined for signs and symptoms of DVT or pulmonary embolism. On an intention-to-treat analysis, DVT occurred in 14.6% of patients receiving Org 10172 and in 19.8% of those receiving heparin during the treatment period (p = 0.392, NS). Pulmonary embolism was diagnosed in one patient in each group. Major conversion to a symptomatic haemorrhagic brain infarct was found in one patient in each group. Death occurred in 13.5% of patients treated with Org 10172 and in 6.7% of patients treated with heparin (p = 0.135, NS). Deaths were mainly related to pulmonary infection and cerebral oedema, thus considered to be due directly to the clinical status of the patients. 1250 anti-Xa Units of Org 10172 once daily is both safe and as effective as 5000 IU of heparin sodium twice daily given for DVT prophylaxis in patients with acute ischaemic stroke of recent onset.

Aged↗

Midbrain ischemia presenting as vertical gaze palsy: value of diffusion-weighted magnetic resonance imaging.

BACKGROUND: Conventional magnetic resonance imaging may fail to identify very small but clinically relevant acute subcortical brain infarcts. Diffusion-weighted magnetic resonance imaging (DWI) is very sensitive and specific for acute cerebral ischemia and should contribute to the early detection of such lesions. METHODS: We analyzed 6 patients who presented with acute vertical gaze palsy and in whom DWI was performed within 1-6 days from symptom onset. RESULTS: DWI accurately identified ischemia in an area supplied by the posterior thalamosubthalamic paramedian artery in all patients. T(2)-weighted and FLAIR imaging failed to identify the clinically relevant lesion in 2 and 3 patients, respectively. CONCLUSION: DWI improves the clinicoanatomical correlation in patients presenting with supranuclear oculomotor disturbances.

Acute Disease↗

Long-lasting regeneration after ischemia in the cerebral cortex.

BACKGROUND AND PURPOSE: Because fibroblast growth factor 2 is a mitogen for central nervous system stem cells, we explored whether long-term fibroblast growth factor 2 delivery to the brain can improve functional outcome and induce cortical neurogenesis after ischemia. METHODS: Rats underwent permanent distal middle cerebral artery occlusion resulting in an ischemic injury limited to the cortex. We used an adeno-associated virus transfection system to induce long-term fibroblast growth factor 2 expression and monitored behavioral and histological changes. RESULTS: Treatment increased the number of proliferating cells and improved motor behavior. Neurogenesis continued throughout 90 days after the ischemia, and the occurrence of newly generated cells with characteristics of neural precursors and immature neurons was most evident 90 days after treatment. CONCLUSIONS: Focal cortical ischemia elicits an ongoing neurogenic response that can be enhanced with fibroblast growth factor 2 leading to improved functional outcome.

Animals↗

Dihydrolipoate reduces neuronal injury after cerebral ischemia.

It has been shown in vitro that dihydrolipoate (DL-6,8-dithioloctanoic acid) has antioxidant activity against microsomal lipid peroxidation. We tested dihydrolipoate for its neuroprotective activity using models of hypoxic and excitotoxic neuronal damage in vitro and rodent models of cerebral ischemia in vivo. In vitro, neuronal damage was induced in primary neuronal cultures derived form 7-day-old chick embryo telencephalon by adding either 1 mM cyanide or 1 mM glutamate to the cultures. Cyanide-exposed and dihydrolipoate-treated (10(-9)-10(-7) M) cultures showed an increased protein and ATP content compared with controls. The glutamate-exposed cultures treated with dihydrolipoate (10(-7)-10(-5) M) showed a decreased number of damaged neurons. In vivo, dihydrolipoate treatment (50 and 100 mg/kg) reduced brain infarction after permanent middle cerebral artery occlusion in mice and rats. Dihydrolipoate treatment (50 and 100 mg/kg) could not ameliorate neuronal damage in the rat hippocampus or cortex caused by 10 min of forebrain ischemia. A comparable neuroprotection was obtained by using dimethylthiourea, both in vitro (10(-7) and 10(-6) M) and at a dose of 750 mg/kg in the focal ischemia models. Lipoate, the oxidized form of dihydrolipoate, failed to reduce neuronal injury in any model tested. We conclude that dihydrolipoate, similarly to dimethylthiourea, is able to protect neurons against ischemic damage by diminishing the accumulation of reactive oxygen species within the cerebral tissue.

Animals↗

Masking of vertebral artery dissection by severe trauma to the cervical spine.

STUDY DESIGN: A prospective case study was performed. OBJECTIVES: To illustrate the association of cervical trauma with vertebral artery dissection, and to propose a diagnostic and therapeutic algorithm for suspected traumatic vertebral artery dissection. SUMMARY OF BACKGROUND DATA: Vertebral artery dissection is a recognized but underdiagnosed complication of trauma to the cervical spine. Symptoms of spinal cord injury, however, may obscure those of vertebral artery dissection, presumably causing gross underdiagnosis of this complication. METHODS: All patients with vertebral artery dissection admitted to the authors' facility between 1992 and 1997 were screened for cervical trauma. RESULTS: This article presents four patients with severe trauma to the cervical spine, defined as luxation, subluxation, or fracture, in whom symptoms of vertebral artery dissection developed after a delay ranging from several hours to weeks. The traumatic vertebral artery dissection typically was located at the site of vertebral injury or cranial to it. One patient with fracture of the odontoid process survived symptom free without ischemic brain infarctions. Another patient survived with traumatic quadriplegia in addition to large cerebellar and posterior cerebral artery infarctions. Two patients died as a result of fulminant vertebrobasilar infarctions, both with only moderate impairment from the primary spinal cord injury. CONCLUSIONS: Early signs of vertebral artery dissection include head and neck pain, often localized to the site of intimal disruption, which may be disguised by the signs of the spinal injury. Early Doppler ultrasound and duplex sonography as a noninvasive screening method should be performed for patients with severe trauma to the cervical spine. In cases of vertebral artery dissection, immediate anticoagulation should be initiated. Traumatologists should be aware of this complication in evaluating patients with severe trauma of the cervical spine, and also for a variety of forensic reasons.

Adult↗

[Cerebrovascular diseases in pregnancy and puerperium].

The incidence, prognosis and causes of strokes associated with pregnancy or puerperium are poorly known, and we do not know whether and to what extent they differ from those of the general female population of childbearing age. Based on early and mostly hospital-based studies, it has been claimed that pregnancy increases the likelihood of cerebral infarction to about 13 times the rate expected outside of pregnancy. However, because of methodological weaknesses, these estimates must be regarded with caution. In a recent study in Ile de France, the incidence of arterial ischemic strokes associated with pregnancy or early puerperium was 4.3 per 100,000 deliveries (95% confidence interval, 2.4 to 7.1), a rate not much different from that for all women of childbearing age. Ischemic strokes related to various etiologies have been reported in pregnancy and the puerperium. Their relative frequency is poorly known because there are no recent large series of pregnancy-related ischemic strokes benefiting from detailed investigation with modern imaging techniques. Most of the known causes of ischemic stroke in the young been reported during pregnancy. In most of these conditions, it is uncertain whether pregnancy is coincidental or plays a role in the occurrence of stroke. Among pregnancy-specific causes, eclampsia may be associated with focal neurological deficits of sudden onset, consistent with a clinical diagnosis of stroke. However, the precise pathogenesis of these stroke-like focal deficits remains poorly understood. Except for some women who have persisting neurological deficits and neuroradiological abnormalities suggesting brain infarction, the reversibility of the neurological clinical signs and neuroradiological lesions within a few days or weeks in most cases argues against the existence of true cerebral ischemic necrosis. The two other pregnancy-specific causes-choriocarcinoma and amniotic fluid embolism-are rarely responsible for focal cerebral ischemia. Other diseases such as peripartum cardiomyopathy and postpartum cerebral angiopathy were initially considered as pregnancy-specific causes but subsequently reported outside of pregnancy. In a significant number of patients, the cause of the stroke remains undetermined, despite an extensive etiological workup. Whether hypercoagulable state and vessel wall changes associated with pregnancy may play a role in the occurrence of these otherwise unexplained ischemic strokes remains unknown. Too frequently, the stroke is considered at the first attempt as a complication of pregnancy and another underlying etiology may be missed. Therefore, evaluation of arterial ischemic stroke in pregnancy should proceed as in the non-pregnant state. There are no follow-up studies that consider the risk of recurrent stroke in future pregnancies. No data are available on the risk associated with use of oral contraception in a woman who had ischemic stroke during pregnancy. The frequency of cerebral venous thrombosis associated with pregnancy and the puerperium is not precisely known. Indeed, epidemiologic studies have been difficult to perform because cerebral venous thrombosis may have a misleading presentation and a definite diagnosis requires angiography, MRI or autopsy. The incidence of cerebral venous thrombosis has been estimated at 10 to 20 per 100000 deliveries in occidental countries, whereas rates of 200 to 500 per 100,000 deliveries have been reported in India. The pregnant and puerperal state accounts for 5 to 20% of all cerebral venous thrombosis in occidental countries; this proportion may reach 60% in developing countries. Labor and delivery are characteristically normal in occidental countries. The occurrence of cerebral venous thrombosis is clearly linked to the puerperial state, suggesting a direct role of the puerperial state.(ABSTRACT TRUNCATED)

Cerebrovascular Disorders↗

Bifrontal measurements of brain tissue-PO2 in comatose patients.

The purpose of this study was to compare brain tissue-PO2 (PtiO2) in lesioned vs. non-lesioned brain tissue. PtiO2 was monitored bifrontally with a "Clark"-type microcatheter in patients following severe head injury (n = 6) and subarachnoid hemorrhage (SAH) (n = 1) from day 2 to day 12 posttrauma/post SAH. Mean arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure and end-tidal CO2 were monitored. Data were stored and analyzed by a multimodal cerebral monitoring system. The CT of five patients was classified as "diffuse injury" and of one patients as "evacuated mass lesion". The patient with SAH (Hunt and Hess IV) had a concomitant intracerebral hematoma which was removed. In all cases, one catheter was placed close to the lesion, while the other was situated in an area with no visible pathology. For analysis, bifrontal PtiO2 data were taken from both on-line monitoring and O2 reactivity tests (FiO2 1.0 for 10 min). Two different patterns were identified: periods of concordance (22% of recordings) and periods in which PtiO2 was lower in lesioned cerebral white matter (78%) but always running parallel. In the latter case, O2-reactivity response was markedly reduced on the lesioned side. Our findings demonstrate a decreased PtiO2 and a reduced O2 reactivity in contused or infarcted brain tissue. Future studies have to clarify which PtiO2 is more important to be used as a guide for therapy.

Brain Concussion↗

Enriched environment after focal cortical ischemia enhances the generation of astroglia and NG2 positive polydendrocytes in adult rat neocortex.

Environmental enrichment (EE) alleviates sensorimotor deficits after brain infarcts but the cellular correlates are not well-known. This study aimed to test the effects of postischemic EE on neocortical cell genesis. A neocortical infarct was caused by distal ligation of the middle cerebral artery in adult spontaneously hypertensive rats, subsequently housed in standard environment or EE. Bromodeoxyuridine (BrdU) was administered during the first postischemic week to label proliferating cells and BrdU incorporation was quantified 4 weeks later in the periinfarct, ipsilateral medial and contralateral cortex. Immunohistochemistry and confocal microscopy were used to analyze co-localization of BrdU with neuronal (calbindin D28k, calretinin, parvalbumin, glutamic acid decarboxylase, tyrosine hydroxylase), astrocytic (glial fibrillary acidic protein, glutamine synthetase, vimentin, nestin), microglia/macrophage (CD11b/Ox-42, CD68/ED-1), oligodendrocyte progenitor/polydendrocyte (NG2, platelet-derived growth factor alpha receptor) or mature oligodendrocyte (myelin basic protein) markers. BrdU positive cells were increased in all analyzed cortical regions in stroke EE rats compared with stroke standard environment rats. Newly born cells in the periinfarct cortex were mostly reactive astroglia. Occasionally, BrdU positive cells in the periinfarct cortex that were negative for glial or microglia/macrophage markers co-expressed markers typical for interneurons but did not express appropriate functional markers. The majority of BrdU positive cells in intact cortical regions, ipsi- and contralaterally, were identified as NG2 positive polydendrocytes. Perineuronally situated newly born cells and polydendrocytes were found to be brain-derived neurotrophic factor immunoreactive. In conclusion, EE enhanced newborn glial scar astroglia and NG2+ polydendrocytes in the postischemic neocortex which might be beneficial for brain repair and poststroke plasticity.

Animals↗

Writer's cramp and tremor due to brain tumor.

Writer's cramp is frequently associated with hand tremor and with other focal dystonias. Sometimes brain infarction, haemorrhage, arterio-venous malformations or tumors are found to cause symptomatic focal dystonias. A 44-year-old man came to our attention due to writer's cramp of his right hand and postural 6-8 Hz tremor. About three months after the onset of the disease the tremor and dystonia disappeared, while a right hemiparesis gradually appeared. Cranial computed tomography showed a hypodense nonhomogeneous lesion in the left cerebral hemisphere parietally, that was assumed to represent a cystic tumor. The patient underwent craniotomy and the histological diagnosis revealed an astrocytoma (Grade II-III). In conclusion our findings confirm the common anatomical basis of symptomatic focal dystonia and tremor. Both can appear after disruption of the pathways within and adjacent to the basal ganglia.

Adult↗

[Study on homocysteine metabolism related enzymes gene mutations in Chinese patients with ischemic cardiovascular and cerebrovascular diseases].

OBJECTIVE: To explore the significance of gene mutations of cystathionine beta-synthase (CBS844ins68), methionine synthase (MS A2756G) and methylenetetrahydrofolate reductase (MTHFR C677T) in ischemic cardiovascular and cerebrovascular diseases. METHODS: The genotypes of CBS 844ins68, MS A2756G and MTHFR C677T were determined by PCR-based assay in 102 patients with brain infarction, 73 with myocardial infarction and 100 healthy controls. RESULTS: The prevalences of CBS 844ins68 and MS A2756G in the cohort studied were somewhat lower than that in western Caucasian populations. There were no significant differences in the frequencies of CBS 844ins 68, MS A2756G and MTHFR C677T mutations between the patient the and control groups. However, the heterozygous form of CBS 844ins 68 tended to be more prevalent in the controls than in the patients. CONCLUSION: Gene mutations as CBS 844ins 68, MS A2756G and MTHFR C677T may not be independent risk factors for ischemic cardiovascular and cerebrovascular disease in Southern Chinese Han population. The prevalences of CBS 844ins 68 and MS A2756G may vary with different ethnic groups or geographic regions.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

Alcohol use and risk of ischemic stroke among older adults: the cardiovascular health study.

BACKGROUND AND PURPOSE: The association of light to moderate alcohol consumption with risk of ischemic stroke remains uncertain, as are the roles of potentially mediating factors and modification by apolipoprotein E (apoE) genotype. METHODS: We studied the prospective association of alcohol consumption and risk of ischemic stroke among 4410 participants free of cardiovascular disease at baseline in the Cardiovascular Health Study, a population-based cohort study of older adults from 4 US communities. Participants reported their consumption of alcoholic beverages yearly. RESULTS: During an average follow-up period of 9.2 years, 434 cases of incident ischemic stroke occurred. Compared with long-term abstainers, the multivariate relative risks of ischemic stroke were 0.85 (95% CI, 0.63 to 1.13), 0.75 (95% CI, 0.53 to 1.06), 0.82 (95% CI, 0.51 to 1.30), and 1.03 (95% CI, 0.68 to 1.57) among consumers of <1, 1 to 6, 7 to 13, and > or =14 drinks per week (P quadratic trend 0.06). ApoE genotype appeared to modify the alcohol-ischemic stroke relationship (P interaction 0.08), with generally lower risks among drinkers than abstainers in apoE4-negative participants but higher risks among drinkers than abstainers among apoE4-positive participants. We could not identify candidate mediators among lipid, inflammatory, and prothrombotic factors. CONCLUSIONS: In this study of older adults, the association of alcohol use and risk of ischemic stroke was U-shaped, with modestly lower risk among consumers of 1 to 6 drinks per week. However, apoE genotype may modify this association, and even moderate alcohol intake may be associated with an increased risk of ischemic stroke among apoE4-positive older adults.

Aged↗

Pathology and pathophysiology of vascular cognitive impairment. A critical update.

The prevalence, morphology, and pathogenesis of vascular dementia (VaD), recently termed vascular cognitive impairment (VCI), and of mixed dementia (Alzheimer disease associated with vascular encephalopathy) are a matter of discussion and clinical diagnostic criteria for these disorders slow low sensitivity and variable specificity. In Western memory clinic-based series, VaD/VCI is suggested in 8-10% of cognitively impaired elderly subjects. Its prevalence in autopsy series ranges from 0.03% to 58% with reasonable values of 4-10%. It has been related to focal, multifocal or diffuse cortical and/or subcortical microinfarcts and lacunes often affecting strategically important brain areas (thalamus, frontobasal and/or limbic systems), hemispheric white matter lesions and, less often, large brain infarcts. They result from systemic, cardiac or local large or small vessel disease. The pathogenesis of cerebrovascular lesions is multifactorial and their pathophysiology affects neuronal systems involved in cognition, memory, and behavior. Vascular pathology often coexists with Alzheimer disease (AD) and other dementing disorders; 25-60% of dementia cases show both AD and vascular lesions. The lesion patterns in ''pure'' VCI with predominant multiple small (subcortical) lesions related to arteriosclerosis and microangiopathies and in mixed dementia (AD associated with vascular encephalopathy), more often showing large infarcts, suggest different pathogenesis of both types of lesions. Due to the high variability of cerebrovascular pathology and its causative factors no validated neuropathological criteria exist for VCI and mixed dementia. In very old subjects selective hippocampal sclerosis may be associated with multiple other vascular pathologies. Minor cerebrovascular lesions, except for severe amyloid angiopathy, appear not essential for cognitive decline in full-blown AD, while both mild AD-type pathology and small vessel disease may interact synergistically in ''unmasking'' or promoting dementia. AD pathology is significantly less severe in the presence of cerebrovascular lesions. Further studies are needed to validate diagnostic criteria for VaD/VCI and to clarify the impact of vascular lesions on cognitive impairment as a basis for more precise clinical diagnosis, early prevention and management.

Alzheimer Disease↗

Mechanical thrombolysis in ischemic stroke attributable to basilar artery occlusion as first-line treatment.

BACKGROUND AND PURPOSE: To report results of mechanical disruption or retrieval of thrombus as first-line treatment in patients with stroke attributable to occlusion of the basilar artery, in particular regarding efficiency and safety. METHODS: In 12 consecutive patients with acute stroke attributable to basilar occlusion, mechanical disruption or thrombus retrieval using various loop-shaped tools was tried before eventually starting local intra-arterial thrombolysis with recombinant tissue plasminogen activator (r-tPA). Main inclusion criteria were: National Institutes of Health Stroke Scale score >8 or Glasgow Coma Scale score <12; onset or worsening of symptoms <8 hours; no hemorrhages or large hypodensities on computed tomography scan; and occlusion of the basilar artery matching clinical symptoms. Efficiency included recanalization, procedure time, and r-tPA dose; safety was defined as rate of procedure-related complications. Outcome was evaluated at 3 months. RESULTS: Mechanical recanalization was successful in 6 patients. A single brain infarction, possibly attributable to distal embolization, occurred. Three patients had good outcomes. In 5 of 6 remaining patients, the artery was recanalized using r-tPA. A single asymptomatic hemorrhage occurred; 3 patients had good outcomes. Procedure time and r-tPA were significantly less in patients with successful mechanical thrombolysis (43.33 minutes and 13.33 mg versus 112.33 minutes and 55.83 mg, respectively). CONCLUSIONS: Mechanical recanalization was effective in half of the patients and at least as safe as local intra-arterial thrombolysis. It allowed to save r-tPA and time. Although the low success rate remains a limit, the excellent and quick anatomical recanalization obtained after successful procedures makes this approach promising.

Adult↗

High-intensity transient signals in patients with cerebral ischemia.

BACKGROUND AND PURPOSE: This study investigated the diagnostic relevance of transcranial Doppler monitoring for the detection of high-intensity transient signals (HITS) in patients with recent cerebral ischemic events of various origins. METHODS: We prospectively performed bilateral transcranial Doppler monitoring (mean, 48 +/- 8 minutes) from both middle cerebral arteries in 280 patients with an acute (< 4 weeks) cerebral ischemic event in the middle cerebral artery territory and in 118 asymptomatic control subjects. HITS were analyzed according to a standardized protocol. RESULTS: Symptomatic patients had a significantly (P < .001) higher rate (9.3%) of HITS than asymptomatic control subjects (1.7%). Patients with reversible ischemia (4.2%) and patients with suspected small-vessel syndromes (4.5%) had lower rates of HITS (P < .05) than those with large-vessel territory strokes (14.2%). Brain imaging (CT/MRI) results corresponded with this observation: the occurrence of HITS was significantly higher (P < .001) in patients with a pattern of large-vessel territorial brain infarction (19.0%) than in those with lacunar lesions (0%) or unidentified ischemic lesions (3.4%). Patients with identified sources of potential embolism (12.9%) had HITS (P < .001) more frequently than those without (0%). Patients with cardiac sources of embolism (excluding artificial heart valves) showed fewer HITS (6.2%) than patients with vascular sources (17.1%). CONCLUSIONS: The results indicate that HITS occur predominantly in patients with large-vessel territory stroke patterns and persisting deficits that are most likely due to artery-to-artery or cardiogenic embolism. In contrast, patients with small-vessel disease and rapid recovery only occasionally present with HITS. Thus, the detection of HITS may substantially support the classification of the individual pathogenesis of cerebral ischemia, particularly when multiple risk constellations for stroke coexist.

Adult↗