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Two cases of brain stem infarction as an early and fatal complication of giant-cell arteritis are reported. These complications occurred despite adequate treatment with corticosteroids. The findings at autopsy are compared with those of the literature. The possible pathogenetic mechanisms of vertebro basilar occlusion and the therapeutical implications are discussed.
A case of brain stem infarction after chiropractic manipulation of the cervical spine is presented. Proposed mechanisms and sites of possible arterial injury are discussed. A diagnosis of vertebral artery occlusion was made using conventional brachial angiography. Digital intravenous angiography, a relatively new and less invasive vascular imaging technique which was used as an adjunct for evaluating the remainder of the cervicocephalic vessels, documented the vertebral occlusion. Chiropractic manipulation, which is increasing in popularity, may be a cause of potentially devastating neurologic disease.
BACKGROUND AND PURPOSE: The study aimed to investigate the predictive value of neurobiochemical markers of brain damage (protein S-100B and neuron-specific enolase [NSE]) with respect to early neurobehavioral outcome after stroke. METHODS: We investigated 58 patients with completed stroke who were admitted to the stroke unit of the Department of Neurology at Magdeburg University. Serial venous blood samples were taken after admission and during the first 4 days, and protein S-100B and NSE were analyzed by the use of immunoluminometric assays. In all patients, lesion topography and vascular supply were analyzed and volume of infarcted brain areas was calculated. The neurological status was evaluated by a standardized neurological examination and the National Institutes of Health Stroke Scale (NIHSS) on admission, at days 1 and 4 on the stroke unit, at day 10, and at discharge from the hospital. Comprehensive neuropsychological examinations were performed in all patients with first-ever stroke event and supratentorial brain infarctions. Functional outcome was measured with the Barthel score at discharge from the hospital. RESULTS: NSE and protein S-100B concentrations were significantly correlated with both volume of infarcted brain areas and NIHSS scores. Patients with an adverse neurological outcome had a significantly higher and significantly longer release of both markers. Neuropsychological impairment was associated with higher protein S-100B release, but this did not reach statistical significance. CONCLUSIONS: Serum concentrations and kinetics of protein S-100B and NSE have a high predictive value for early neurobehavioral outcome after acute stroke. Protein S-100B concentrations at days 2 to 4 after acute stroke may provide valuable information for both neurological status and functional impairment at discharge from the acute care hospital.
PURPOSE: To study the reliability of brain infarct volume assessment with ruler and calculator. METHODS: The brain infarctions of 45 patients were measured using 3 different methods on CT scans: In each section showing the lesion, the largest diameters were measured and multiplied by the slice thickness using the formula for A) an ellipsoid and B) a cylinder. The sectional volumes were summed up to calculate the entire lesion volume. C) Using the ellipsoid formula, the thickness of all sections showing the lesion were added and used as the third diameter which was multiplied with the two largest diameters of the lesion. The lesion volume was also assessed by planimetry on a workstation and served as reference. Using method A, two independent investigators measured 93 brain infarcts of 49 patients to assess the 95% confidence interval (CI) of agreement. RESULTS: Compared to the reference, method A underestimated the volumes by -25%, method B overestimated the volumes by +12.5%, and method C by +18.6%. The mean difference between the two investigators was 2 ml. The 95% CI for small infarcts < or = 50 ml was 60%-150%, for larger infarcts +/- 26 ml. CONCLUSION: This simple method is only reliable when changes in infarct volume exceeding 26 ml are to be detected.
1. The polymorphonuclear neutrophils (PMN) activation and mobilization observed in acute cerebral infarction contribute to the brain tissue damage, but PMN could also be involved in postischemic functional injury of ischemied blood vessel. 2. This study was undertaken to investigate whether pharmacological neutropenia could modify the postischemic endothelial dysfunction in comparison to smooth muscle whose impairment is likely more related to reperfusion and oxidative stress. 3. A cerebral ischemia-reperfusion by endoluminal occlusion of right middle cerebral artery (MCA) was performed 4 days after intravenous administration of vinblastine or 12 h after RP-3 anti-rat neutrophils monoclonal antibody (mAb RP-3) injection into the peritoneal cavity, on male Wistar rats with 1-h ischemia then followed by 24-h reperfusion period. Brain infarct volume was measured by histomorphometric analysis and vascular endothelial and smooth muscle reactivity of MCA was analysed using Halpern myograph. 4. Neutropenia induced a neuroprotective effect as demonstrated by a significant decrease of brain infarct size. In parallel to neuroprotection, neutropenia prevented postischemic impairment of endothelium-dependent relaxing response to acetylcholine. In contrast, smooth muscle functional alterations were not prevented by neutropenia. Ischemia-reperfusion-induced myogenic tone impairment remained unchanged in vinblastine and mAb RP-3-treated rats. Postischemic Kir2.x-dependent relaxation impairment was not prevented in neutropenic conditions. The fully relaxation of smooth muscle response to sodium nitroprusside was similar in all groups. 5. Our results evidenced the dissociate prevention of pharmacologically induced neutropenia on postischemic vascular endothelial and smooth muscle impairment. The selective endothelial protection by neutropenia is parallel to a neuroprotective effect suggesting a possible relationship between the two phenomena.
The value of contrast enhancement for the diagnosis of the ischemic brain infarct is discussed critically. In some publications there were hints to possible deterioration of the clinical prognosis of patients with brain infarcts if contrast medium had invaded into the brain parenchyma. The pathophysiological base is briefly discussed. The leading idea is the restrictive use of the contrast medium. Our opinions of different publications are controversial, and therefore useless for the diagnostic consequences. We have gained by working out detailed rules for the indication of a intravasal contrast application in patients with brain infarcts.
BACKGROUND AND PURPOSE: We studied six patients suffering from pure, unilateral brain stem infarction to explore the association of remote cerebral and cerebellar blood flow changes with damage at different sites of this region of the brain. METHODS: We used single-photon emission computed tomography and [123I]iodoamphetamine to measure regional differences in tracer uptake. Qualitative image analysis and calculated asymmetry indexes were correlated to the location of the infarcted area on magnetic resonance imaging and to the patients' clinical findings. RESULTS: Significant perfusion asymmetries were noted in the two patients with infarction in the upper pons but not in those with lesions below this level. They comprised a contralateral cerebellar and ipsilateral supratentorial hypoactivity that was most marked in the frontoparietal cortex. There was no clear relation between the patterns of cerebral or cerebellar tracer uptake and specific neurological findings. CONCLUSIONS: Remote perfusion changes after pure brain stem infarction may be seen both infratentorially and supratentorially and depend on the lesion site rather than on the neurological deficit. In this context, our study confirmed damage to the corticopontocerebellar pathways as the key event in the genesis of a crossed cerebellar diaschisis. The exact mechanisms causing ipsilateral cerebral hemispheric diaschisis await further clarification.
The association between cerebral small-vessel disease, brain atrophy, and the risk and severity of mild parkinsonian signs (MPS) remains unclear. The objective of this study is to examine the effect of lacunar brain infarcts, cerebral white matter lesions (WMLs), and cortical atrophy on the risk and severity of MPS. This study is a cross-sectional community-based cohort study comprising 268 subjects, 65 to 83 years of age, residing in the Augsburg region of southern Germany, and without contraindications for magnetic resonance imaging (MRI) of the brain. Main outcome measures. Subcortical and periventricular WMLs, lacunar brain infarcts, and cortical atrophy determined using a standardized MRI protocol developed for the Rotterdam Scan Study and an established rating scale. MPS, assessed in a standardized neurological examination and based on the Unified Parkinson's Disease Rating Scale motor scale. Lacunar brain infarcts and large subcortical white matter lesions were associated with an elevated risk of resting tremor. More severe cortical atrophy was related to an increased risk of rigidity and bradykinesia. In a linear regression analysis relating each individual MRI measurement with the severity of MPS, the number of lacunar brain infarcts and the degree of brain atrophy were correlated with the severity of resting tremor, whereas the size of subcortical and periventricular WMLs was correlated with the severity of rigidity. A higher degree of brain atrophy was associated with increased severity of either cardinal sign. In our study, presence and volume of lacunar brain infarcts, cerebral WMLs, and cortical atrophy were associated with the risk as well as severity of MPS. Determining the presence of these brain changes using brain imaging might contribute to identify persons at risk for MPS.
BACKGROUND AND PURPOSE: The role of recent heavy drinking of alcohol as a risk factor for ischemic brain infarction is unclear. We investigated this problem in young adults, in whom even a thorough workup often fails to reveal any predisposing factor. METHODS: This was a hospital-based case-control study comprising 75 consecutive subjects aged 16 to 40 years with first-ever ischemic brain infarction and 133 control subjects from the same hospital who were group-matched with the case patients for age, sex, day of the onset of symptoms, and acuteness of disease onset. RESULTS: Multiple logistic regression analysis showed that alcohol intake exceeding 40 g of ethanol within the 24 hours preceding disease onset was a significant independent risk factor for brain infarction among both men (odds ratio [OR], 6.0; 95% confidence interval [CI], 1.8 to 20.3) and women (OR, 7.8; 95% CI, 1.0 to 60.8). Cigarette smoking was not found to be an independent risk factor in the model, whereas among men arterial hypertension was (OR, 6.2; 95% CI, 1.5 to 24.7). CONCLUSIONS: We conclude that very recent alcohol drinking, particularly drinking for intoxication, may trigger the onset of brain infarction in young adults and that there might be a variety of mechanisms behind this effect.
BACKGROUND AND PURPOSE: The influence of stroke subtype on recurrence, and determinants of recurrence-free survival after a first-ever stroke are not fully understood. We aimed to clarify the long-term prognosis by stroke subtypes and to identify determinants for recurrence and death after a first-ever stroke. METHODS: We enrolled 1,732 consecutive patients (men/women = 1,134/598, mean age of 65 years) with a first-ever acute stroke who were admitted to our Stroke Care Unit during a period of 20 years. Stroke subtypes were classified as atherothrombotic brain infarction, lacunar infarction, cardioembolic infarction, other type of infarction, and brain hemorrhage. The prognosis was assessed by stroke subtypes. RESULTS: During the hospital stay (mean 61 days), 99 patients died: 73 died directly from stroke. A total of 198 patients had recurrent strokes, and 286 died within 3 years after the index stroke. The overall recurrence rate within the first year was 6.5%, which was different among stroke subtypes. Patients with cardioembolic infarction (9.0%) as well as other type of infarction (9.1%) had more recurrent strokes within the initial year compared with the other subtypes. A history of transient ischemic attack (relative risk = 1.38), atrial fibrillation (1.52), ischemic heart disease (1.40), and disability at discharge (2.64) were independent predictors for the recurrence and death within 3 years after the first-ever stroke. CONCLUSIONS: The recurrence rate was different among stroke subtypes within 1 year after the index stroke. Atrial fibrillation, ischemic heart disease, history of transient ischemic attack, and disability at discharge were important determinants for stroke recurrence and death.
Two patients sustained an ischemic brain stem infarction during medical examination and treatment. The first patient lost consciousness and the spontaneous respiration ceased during X-ray examination of the cervical spine when the neck was hyperextended. After some minutes he regained conciousness but was found to be tetraplegic, and the patient deceased 4 months later. The angiogram revealed thrombosis of the basilar artery. The other patient had profuse nosebleed and was treated with posterior tamponation during which she sat for about 10 min with the neck hyperextended. Some hours after this procedure symptoms and signs of lateral caudal brain stem infarction emerged.
Glial cell line-derived neurotrophic factor (GDNF) is a transforming growth factor-beta which has shown beneficial effects in rats after acute focal cerebral ischemia (FCI). To study the effects of GDNF on chronic FCI injury in conscious rats, we used fibrin glue (GDNF-fibrin glue) and fibrin glue free (GDNF-only)-GDNF topically applied to the ischemic brain after right middle cerebral artery (MCA) ligation. Infarct brain volume and functional motor deficits were measured before and after FCI injury. After FCI injury induced by right MCA ligation, rats were randomly assigned to one of four treatment groups: (a) sham, (b) control, (c) topically applied GDNF (1 mug)-only, and (d) topically applied GDNF (1 mug)-fibrin glue. The degree of ischemic brain injury was estimated by infarct volume of right MCA territory at 4 weeks after occlusion. The functional motor deficits were quantified with rotarod test and grasping power test once a week. Topically applied GDNF-fibrin glue at infarct brain tissue after 4 weeks FCI injury significantly reduced the total infarct volume by 44.3% and 36%, respectively, compared to that of control group and GDNF-only group. The mean latencies for rats to stay on the rotarod were 55.0%, 50.3%, and 92.2% (P < 0.05 vs. control group and GDNF-only group) of baseline, respectively, in the control, GDNF-only, and GDNF-fibrin glue groups at the end of the 1st week after FCI injury but 75.3%, 67.3%, and 106.6% (P < 0.05 vs. control group and GDNF-only group) of baseline at the end of the 4th week after FCI injury. The mean values of grasping power were 78.7%, 71.7%, and 101.2% (P < 0.05 vs. control group and GDNF-only group) of baseline, respectively, in the control, GDNF-only, and GDNF-fibrin glue groups at the end of 1st week after FCI injury but 89.6%, 97.6%, and 120.7% (P < 0.05 vs. control group) of baseline at the end of 4th week after FCI injury. These results indicate that GDNF-fibrin glue not only reduced the total infarct volume after FCI injury but can also improve motor deficits after FCI injury. We concluded GDNF-fibrin glue could facilitate delivery of GDNF to the damaged brain tissue with subsequent reduction of ischemic brain injury accompanied by enhancing functional recovery in rats with chronic FCI injury.
BACKGROUND AND PURPOSE: The right-to-left shunt from pulmonary arteriovenous fistula (P-AVF) with Rendu-Osler-Weber (R-O-W) disease can cause paradoxical brain embolism. However, it has remains unclear whether the isolated P-AVF without Rendu-Osler-Weber (R-O-W) disease is associated with ischemic stroke, in particular, paradoxical brain embolism. Our group previously reported a case with paradoxical brain embolism associated with isolated P-AVF without R-O-W disease in 1996. Furthermore, in 1999, we reported that transcranial Doppler (TCD) with saline contrast medium was useful for identifying the presence of P-AVF as a right-to-left shunt. Therefore, when we have an embolic stroke patient with unknown source, we have performed TCD for detecting P-AVF since 1998. The aim of this study was to investigate the frequency of brain infarction associated with isolated P-AVF without R-O-W disease and to evaluate clinical characteristics including a previously reported case, and to elucidate the stroke mechanism. METHOD AND SUBJECTS: We studied patients with brain infarction associated with isolated P-AVF without R-O-W disease from 642 ischemic stroke patients admitted to our group within 7 days of stroke onset between August 1998 and May 2002. RESULTS: Four patients (0.6%) was diagnosed as having brain infarction associated with isolated P-AVF without R-O-W disease. Clinical characteristics of 5 patients were as follows; 1) all patients were middle aged women (mean, 61 year old), 2) they had no evidences of chronic hypoxia such as cyanosis, dyspnea, and erythrocytosis, 3) all strokes occurred in the morning, 4) the diagnosis of brain embolism was made by routine neuroimaging studies, but no potential cardiac nor arterial sources of emboli were detected, 5) the location of brain infarcts on MRI was more frequently in vertebrobasilar circulation (4 cases) than in carotid circulation (1 case), 6) all patients had pulmonary embolism and 4 suffered from deep venous thrombosis, 7) all patients had a history of brain infarction or transient ischemic attack (TIA) before the present attack, 8) all patients had a single P-AVF and its location was right lower lobe in 4 patients and the left lower lobe in the remaining one patient, and 9) all patients could be treated with catheter embolization of P-AVF without recurrent stroke for 37 months in average (range 2-100 months). CONCLUSION: The isolated P-AVF without R-O-W disease can cause paradoxical brain embolism. Catheter embolization of P-AVF may be effective in prevention for recurrent stroke. We should not overlooked isolated P-AVF as a right-to-left shunt in embolic stroke patients with unknown etiology.
PURPOSE: To explore the frequency and patterns of brain infarction and other brain manifestations in cervicocephalic artery dissection (CCAD) and to evaluate the correlation between vessel wall findings and infarctions. MATERIAL AND METHODS: The medical records and films of 136 consecutive CCAD patients diagnosed in Oulu University Hospital during the 20-year period since 1982 were reviewed. Five patients with no brain imaging were excluded. RESULTS: One-hundred-and-twenty-seven patients underwent cerebral CT and four patients MRI. Brain infarction was detected in 73 patients (56%), 43 of whom had cerebral infarction associated with anterior circulation dissection and 30 cerebellar infarction associated with posterior circulation dissection. Occlusion of the dissected vessel was accompanied by infarction in 76%, irregular stenosis in 40%, and other findings in 12%. Of the anterior circulation infarctions, territorial and subcortical infarctions and territorial infarctions with fragmentation, which are considered embolic, accounted for 95%, while only 5% were in the watershed area and considered hemodynamic. Intracranial posterior circulation dissection rarely caused infarction (in 1/11 of the dissected vessels), whereas intracranial anterior circulation dissection resulted in infarction more commonly (9/12). Altogether 23% of patients with intracranial CCAD had subarachnoid hemorrhage. Hemorrhagic transformation was present in five patients. CONCLUSIONS: More than half of CCAD patients have cerebral or cerebellar infarction at CT or conventional MR imaging. Occlusion of the dissected vessel is accompanied by infarction more often than other vessel wall abnormalities. Most cerebral infarctions caused by arterial dissections are of embolic origin. Intracranial dissections cause subarachnoid hemorrhage in more than 20% of patients.
The neuroprotective effects of minocycline-which is broadly protective in neurologic-disease models featuring cell death and is being evaluated in clinical trials-were investigated both in vitro and in vivo. For the in vivo study, focal cerebral ischemia was induced by permanent middle cerebral artery occlusion in mice. Minocycline at 90 mg/kg intraperitoneally administered 60 min before or 30 min after (but not 4 h after) the occlusion reduced infarction, brain swelling, and neurologic deficits at 24 h after the occlusion. For the in vitro studies, we used cortical-neuron cultures from rat fetuses in which neurotoxicity was induced by 24-h exposure to 500 microM glutamate. Furthermore, the effects of minocycline on oxidative stress [such as lipid peroxidation in mouse forebrain homogenates and free radical-scavenging activity against diphenyl-p-picrylhydrazyl (DPPH)] were evaluated to clarify the underlying mechanism. Minocycline significantly inhibited glutamate-induced cell death at 2 microM and lipid peroxidation and free radical scavenging at 0.2 and 2 microM, respectively. These findings indicate that minocycline has neuroprotective effects in vivo against permanent focal cerebral ischemia and in vitro against glutamate-induced cell death and that an inhibition of oxidative stress by minocycline may be partly responsible for these effects.
OBJECTIVE: To define therapeutic strategy for management of patients with ischemic stroke due to a high probability of paradoxical embolism through a Patent Foramen Ovale (PFO). METHODS: Since 1988 all consecutive patients with cerebrovascular events and PFO from the Stroke Registry of our population-based primary-care center are prospectively studied and followed. Since 1992, among 118 patients with cryptogenic embolic brain infarct or transient ischemic attack (TIA) and PFO, 32 consecutive patients younger than 60 years who presented at least two of the following criteria were admitted for surgery: history of Valsalva strain before stroke (11); multiple clinical events (13); multiple infarcts on brain Magnetic Resonance Imaging (MRI) (15); atrial septal aneurysm (ASA) (16); large right-to-left shunt (> 50 microbubbles) (12). RESULTS: Operative time 135' +/- 33'. CPB time 34' +/- 14'. Aortic crossclamping time 16' +/- 6'. Post-operative bleeding 485 +/- 170 ml. No homologous blood transfusion required. No neurological, cardiac or renal complications. All patients were followed-up corresponding to a cumulative time of 601 patient-months. This revealed no recurrent vascular events nor silent new brain lesions on brain MRI. Systematic simultaneous contrast Trans Esophageal Echocardiography (TEE)-Trans Cranial Doppler showed a small residual interatrial shunt in two patients. CONCLUSION: Surgical closure of a patent foramen ovale can be accomplished with very low morbidity and reduce efficiently the risk of stroke recurrence. It seems to be the option of choice in selected patients with a higher (> 1.5%/year) risk of stroke recurrence.
Brain infarcts and brain hemorrhages in patients younger than 20 years are significantly less common than among those older than 65 years; also, their clinical expressions are different from those common to older patients. Congenital defects involving the heart and the arteries supplying the brain are among the most common causes of stroke in the young. In addition to the structural changes affecting the heart and blood vessels, various genetic disorders (hematologic, mitochondrial, and others) are being identified as significant risk factors in an increasing number of young stroke victims.
Two cases of giant intracavernous aneurysms treated by high flow bypass with saphenous vein graft between the external carotid artery (ECA) and branches of the middle cerebral artery (MCA) are presented. Very often these aneurysms are unclippable because they are fusiform or have a large neck. Occlusion of the internal carotid artery (ICA) is the treatment of choice in many cases. This procedure has however a high risk of brain infarction. Revascularization of the brain by extra-intracranial anastomosis between the superficial temporal artery (STA) and branches of the MCA is frequently performed. This procedure provides however a low flow bypass and brain infarction may occur. We report two cases of giant cavernous sinus aneurysms treated by high flow bypass and endovascular balloon occlusion of the ICA. Immediate high flow revascularization of MCA branches was achieved and the patients showed no ischemic events. Follow-up of 8 and 14 months after operation shows patency of the venous graft and no neurological deficits. Angiographic control examination showed complete aneurysm occlusion in both cases.