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PubMed2002

[Clinical presentation and prognosis of brain stem infarcts. An evaluation of the Stroke Databank of the German Stroke Foundation].

Due to the great variety of clinical classification systems and syndromes, a representative overview of the etiology and prognosis of brain stem infarctions is missing. From the German Stroke Data Bank we therefore investigated 455 patients with visible brainstem infarction on cerebral imaging in comparison to patients with other infarct localizations. Follow-up after 3 and 12 months assessed functional outcome and recurrence of cerebral ischemia. Of 455 patients with acute brainstem infarction, 115 had additional infarctions in other vascular territories. In the remaining 340 patients with isolated brainstem infarction, the classification was: small vessel disease in 36.2%, macroangiopathy in 22.6%, and cardioembolism in 11.2%. After 3 months, 10% of the patients with isolated brainstem infarction had died and 55.6% were functionally independent. Mortality was 43.5% in patients with combined brainstem infarction. Our study highlights the frequency of small vessel disease as well as the relatively favorable prognosis in isolated brainstem infarction and preserved consciousness.

Aged↗
PubMed2000

Delayed treatment with nicotinamide (Vitamin B(3)) improves neurological outcome and reduces infarct volume after transient focal cerebral ischemia in Wistar rats.

BACKGROUND AND PURPOSE: We have previously shown that nicotinamide (NAm) acutely reduces brain infarction induced by permanent middle cerebral artery occlusion (MCAo) in rats. In this study, we investigate whether NAm may protect against ischemia/reperfusion injury by improving sensory and motor behavior as well as brain infarction volumes in a model of transient focal cerebral ischemia. METHODS: Forty-eight male Wistar rats were used, and transient focal cerebral ischemia was induced by MCAo for 2 hours, followed by reperfusion for either 3 or 7 days. Animals were treated with either intraperitoneal saline or NAm (500 mg/kg) 2 hours after the onset of MCAo (ie, on reperfusion). Sensory and motor behavior scores and body weight were obtained daily, and brain infarction volumes were measured on euthanasia. RESULTS: Relative to treatment with saline, treatment with NAm (500 mg/kg IP) 2 hours after the onset of transient focal cerebral ischemia in Wistar rats significantly improved sensory (38%, P<0.005) and motor (42%, P<0.05) neurological behavior and weight gain (7%, P<0.05) up to 7 days after MCAo. The cerebral infarct volumes were also reduced 46% (P<0.05) at 3 days and 35% (P=0.09) at 7 days after MCAo. CONCLUSIONS: NAm is a robust neuroprotective agent against ischemia/reperfusion-induced brain injury in rats, even when administered up to 2 hours after the onset of stroke. Delayed NAm treatment improved both anatomic and functional indices of brain damage. Further studies are needed to clarify whether multiple doses of NAm will improve the extent and duration of this neuroprotective effect and to determine the mechanism(s) of action underlying the neuroprotection observed. Because NAm is already used clinically in large doses and has few side effects, these results are encouraging for the further examination of the possible use of NAm as a therapeutic neuroprotective agent in the clinical treatment of acute ischemic stroke.

Animals↗
PubMed2005

Cerebral infarctions and brain abscess due to Lemierre syndrome.

Lemierre syndrome is characterized by anaerobic bacterial infection in the head and neck, causing thrombophlebitis of the jugular vein and septic metastasis to various distant organs, most often the lungs. Here we describe previously unreported clinical features of cerebral infarctions and brain abscess due to metastatic septic embolism of this uncommon but lethal syndrome, and the successful course of treatment with ampicillin, cefotaxime and metronidazole.

Brain Abscess↗
PubMed2002

Neuroprotective effects of the sodium channel blocker RS100642 and attenuation of ischemia-induced brain seizures in the rat.

Seizurogenic activity develops in many patients following brain injury and may be involved in the pathophysiological effects of brain trauma and stroke. We have evaluated the effects of the use-dependent sodium channel blocker RS100642, an analog of mexiletine, as a neuroprotectant and anti-seizure agent in a rat model of transient middle cerebral artery occlusion (MCAo). Post-injury treatment with RS100642 (0.01-5.0 mg/kg) dose-dependently reduced brain infarction, improved functional recovery of electroencephalographic (EEG) power, and improved neurological outcome following 2 h of MCAo and 24 h recovery. This effect was more potent and offered a larger reduction of brain infarct volume than a maximal neuroprotective dose of mexiletine (10.0 mg/kg). Furthermore, brain seizure activity recorded following 1 h MCAo and 72 h of recovery in injured rats was either completely blocked (30 min pre-MCAo treatment) or significantly reduced (30 min post-MCAo treatment) with RS100642 (1.0 mg/kg) treatment resulting in greater than 60% reduction of core brain infarct. These results indicate that brain seizure activity during MCAo likely contributes to the pathophysiology of brain injury and that RS100642 may be an effective neuroprotective treatment not only to decrease brain injury but also to reduce the pathological EEG associated with focal ischemia.

Animals↗
PubMed1983

[Therapy and prognosis of subarachnoid hemorrhage due to rupture of a cerebral aneurysm].

The morbidity and mortality in 100 consecutive patients, almost all admitted within one week after a proven subarachnoid hemorrhage, were investigated in a prospective study. An aneurysm was demonstrated by angiography or autopsy in 76 patients, while in 24 patients the cerebral panangiography was normal. 13.1% of the patients with a proven aneurysm died within 48 hours of the hemorrhage as a consequence of a massive initial bleeding, 23.6% died from preoperative rebleeding or brain infarcts due to cerebral vascular spasms, 2.6% from direct operative complications and 2.6% from brain infarcts due to postoperative cerebral vascular spasms. The total case mortality was 41.9%. This high mortality was due to massive initial hemorrhage, early rebleedings and in particular to pre- and postoperative brain infarcts due to cerebral vascular spasms. The prognosis can only be improved significantly by early diagnosis and admission and effective prophylaxis and therapy of the vasospasm, but not by further perfecting of surgical technique.

Humans↗
PubMed2002

Comparative neuroprotective effects of preischemic PACAP and VIP administration in permanent occlusion of the middle cerebral artery in rats.

OBJECTIVES: Pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) belong to the same peptide family, and both neuropeptides have been shown to exert in vitro and in vivo neurotrophic and neuroprotective effects. The aim of the present study was to investigate and compare the protective effects of PACAP and VIP in permanent focal cerebral ischemia in rats. The effect on the progression of the cerebral infarct was also studied. METHOD: Male rats were injected 450 pmol PACAP or VIP dissolved in physiological saline intracerebroventricularly, preceding the occlusion of the middle cerebral artery. Control animals received vehicle treatment. Permanent focal ischemia was induced by the intraluminal filament occlusion of the middle cerebral artery. Animals were sacrificed 12 or 24 hours after the onset of ischemia, and infarcted brain areas were determined by staining bran sections with triphenyl-tetrazolium chloride. RESULTS: Twelve hours after ischemia, the infarcted brain volume resulted to be 14.8% in the control group, 15.3% in the VIP-treated group and 5.8% in the PACAP-treated animals. Twenty-four hours after middle cerebral artery occlusion, the infarcted brain volumes were 21.5%, 20.7% and 14.3% in the control, VIP and PACAP-treated animals, respectively. CONCLUSION: Our results provide further evidence for the neuroprotective effects of PACAP38 as given in form of a preischemic bolus. It slows down the progression of the evolution of the infarct and reduces the final infarct size. In contrast, a related peptide, VIP, does not have neuroprotective effects under the same experimental conditions.

Animals↗
PubMed1993

Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat.

Focal brain ischemia induced in rats by occlusion of an intracranial artery is a widely used paradigm of human brain infarct. Details of the structural changes that develop in either the human or the rat brain at various times after occlusion of an intracranial artery are incompletely characterized. We studied, in 48 adult Wistar rats, structural alterations involving the cerebral hemisphere ipsilateral to an arterial occlusion, at intervals ranging from 30 min to 7 days. Microscopic changes developed over time in separate areas of the corresponding cerebral hemisphere in a predictable pattern, appearing as small lesions in the preoptic area (30 minutes), enlarging to involve the striatum, and finally involving the cerebral cortex. Two types of neuronal responses were noted according to the time elapsed; acute changes (up to 6 hours) included scalloping, shrinkage, and swelling, whereas delayed changes (eosinophilia and karyolysis) appeared later (> or = 12 hours). Three types of astrocytic responses were noted. 1) Cytoplasmic disintegration occurred in the preoptic area at a time and in a place where neurons appeared minimally injured. 2) Nuclear and cytoplasmic swelling were prominent responses in the caudoputamen and cerebral cortex at a time when neurons showed minimal alterations. 3) Increased astrocytic glial fibrillary acidic protein reactivity was noted at the interface between the lesion and the surrounding brain tissue after 4 to 6 hours. The gross pattern of the brain lesion and the maturation of neuronal changes typical of a brain infarct have a predictable progression. Focal brain ischemia of up to 6-hour duration does not induce coagulation necrosis.

Animals↗
PubMed1983

[Differential diagnosis of severe forms of cerebral infarct (clinico-echoencephalographic and pathomorphologic study)].

Clinical, echoelectroencephalographic and pathomorphological study in 73 patients with grave ischemic insult in arteria cerebralis media region was performed. Brain infarctions caused by thrombosis were characterized by small M-echo displacement 12 hours after process beginning followed by displacement increase in 3-4 days. Brain infarctions caused by thromboembolic process were characterized by small M-echo displacement 6 hours after accident with subsequent fast increase of displacement till mean or great values in the second half of the first day. Supratentorial brain infarctions not connected with thrombosis were not accompanied by M-echo displacement.

Aged↗
PubMed2004

Computer-assisted characterisation of a carotid plaque.

BACKGROUND: The aim of this study was to attempt an objective assessment of carotid plaque echogenicity by means of computer-aided technique and to determine the association between the echogenicity and the incidence of brain infarctions. MATERIAL/METHODS: 54 carotid plaques causing internal carotid artery stenosis within the range of 60 - 99% constituted the material for our studies. The images of the plaques obtained by means of USG were transferred to and saved on the computer. Using image analysis software, a histogram of each plaque was obtained. The grey scale median (GSM range 0 - 255) for each histogram, which was used as a measure of the plaque echogenicity, was determined. The value of GSM was assessed in patients who suffered from brain infarctions in the area of the stenosed artery and in patients without infarctions. RESULTS: The grey scale median associated with cerebral infarction was nearly two times lower in comparison with GSM of plaques found in patients without infarction. Among 30 plaques with GSM >35,only 5.5%were connected with brain infarction ,and 27.8%of the 24 plaques with GSM <35 were associated with brain infarction.No correlation with cerebral infarction was found for 50%of the plaques with GSM >35 and 16.7%of the plaques with GSM <35. CONCLUSIONS: The use of computer-aided method allows assessment of carotid plaque echogenicity and can be used for clinical studies aimed at evaluation of the correlation between carotid plaque type and a risk of ischemic stroke.

Aged↗
PubMed1995

Cerebral blood flow and metabolism in hypertensive patients with cerebral infarction.

The authors investigated, by positron emission tomography, the effect of long-standing hypertension on cerebral blood flow (CBF) and oxygen metabolism in patients with chronic atherothrombotic brain infarction. In the nonbrain infarct (non-BI) group (n = 13, mean age: sixty-two years), the regional CBF (rCBF) was decreased significantly with a rise in the mean arterial blood pressure (MABP) in the cerebral cortexes (r = -0.575) and the deep gray matter (r = -0.451), whereas the regional cerebral metabolic rate for oxygen (rCMRO2) remained unchanged. In the brain infarct (BI) group (n = 22, mean age: fifty-eight years), however, the rCBF as well as the rCMRO2 were reduced even in the normotensive patients and thus did not correlate with the MABP. These results suggest that long-standing hypertension per se causes a reduction in the rCBF but not in the oxygen metabolism with a compensatory increase in the oxygen extraction fraction. On the other hand, patients with brain infarction, even normotensives, show a diffuse decrease in cerebral circulation and metabolism, which is probably due to the more severe sclerotic changes that take place in the cerebral vessels.

Blood Pressure↗
PubMed2003

Vertebrobasilar artery dissection presenting with simultaneous subarachnoid hemorrhage and brain stem infarction: case report.

BACKGROUND: Intracranial dissecting aneurysms have been associated with subarachnoid hemorrhage (SAH) or cerebral ischemia. We encountered a patient presenting with simultaneous subarachnoid hemorrhage and brainstem infarction caused by a dissecting aneurysm of the vertebrobasilar artery, which was diagnosed by magnetic resonance imaging (MRI) but did not show abnormal findings on cerebral angiography. CASE DESCRIPTION: A 55-year-old man had sudden onset of headache and left abducens palsy. Computed tomography revealed a subarachnoid hemorrhage localized in the left prepontine cistern and the left cerebellomedullary fissure. Cerebral angiography showed neither a saccular aneurysm nor fusiform dilatation causing the subarachnoid hemorrhage. MRI demonstrated a small infarction in the left dorsal pons, and an intramural hematoma of the left vertebral artery and lower basilar artery. CONCLUSION: This is a rare case of a vertebrobasilar dissecting aneurysm that simultaneously caused both SAH and brain stem infarction. MRI should be performed in the acute phase of SAH of unknown origin to determine the possible coexistence of a dissecting aneurysm, as occurred in this case.

Aortic Dissection↗
PubMed2002

Effect of intravenous gadolinium-DTPA on diffusion-weighted images: evaluation of normal brain and infarcts.

BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) is usually done before administration of intravenous contrast agents. Repetition of DWI is occasionally necessary after administration, but the effects of contrast material on DWI and apparent diffusion coefficient (ADC) values have not yet been fully examined. The present study assesses whether administration of gadolinium-based contrast material significantly affects DWI and ADC values. METHODS: We examined DWI data from 39 patients (mean age, 67.9 years; range, 34 to 87 years) who were evaluated with a stroke protocol at our institute. All patients were scanned at the acute or subacute stages of infarct from 3 hours to 5 days after symptom onset. We obtained DWI images using single-shot echo-planar imaging with a b value of 1000 s/mm2. Patients were injected with 0.1 mmol gadopentetate dimeglumine per 1 kg body weight. We examined the signal-to-noise ratio of the normal brain and the infarct and evaluated the contrast-to-noise ratio of each lesion. In addition, we compared the ADC values calculated from the DWI images before and after administration of contrast. The statistical significance of differences between precontrast and postcontrast administration was determined by use of a paired t test. RESULTS: The signal-to-noise and contrast-to-noise ratios of the DW images were not significantly different before and after administration of contrast agent. The ADC values were slightly lower after administration of contrast agent for both normal brain (P=0.0011) and infarcts (P=0.038). The estimated differences in the ADC values were approximately 1.3% and 3.5% for normal brain and infarcts, respectively. CONCLUSIONS: The lack of a significant difference between the signal-to-noise and contrast-to-noise ratios of DW images before and after administration of contrast agent indicates the feasibility of postcontrast DWI.

Adult↗
PubMed1991

Magnetic resonance images of brain stem infarct in periarteritis nodosa.

A 35-year-old woman displayed unusual symptoms of progressive bulbar dysfunction. At necropsy, systemic necrotizing vasculitis and small pontine infarcts were demonstrated. The angiographic and magnetic resonance imaging findings are described. The latter investigation is a sensitive method for detecting such pontine lesions. To our knowledge, this case is the first report of magnetic resonance imaging findings of brain stem infarct in a patient with periarteritis nodosa.

Adult↗
PubMedDate not supplied

Temporal profile (clinical course) of acute vertebrobasilar system cerebral infarction.

Records of 37 consecutive patients with acute brain infarction from vertebrobasilar artery disease, admitted to the cerebrovascular hospital service within 36 hours of the onset of symptoms, were studied to define the temporal profile of clinical events during the first week of illness. A stable course with unchanged neurologic deficit was found in 11% (4 patients). Progressive improvement in symptoms occurred in 35% (13 patients). Progressive disability occurred in 43% (16 patients). A remitting-relapsing course was noted in 11% (4 patients). In these latter 2 groups, stabilization of the clinical course occurred in the majority with 48 hours after the initial symptom; however, definite changes continued to develop up to 96 hours in a significant number of patients. Mortality at the conclusion of the first week was 27% for the entire group. This was 2.5 times greater than the 10.6% previously reported for a group of 179 patients with acute brain infarction due to carotid system disease who were concomitantly studied.

Anticoagulants↗
PubMed2003

[Vertebrobasilar artery dissection with subarachnoid hemorrhage after brain stem infarct showing an improvement on angiography: case report].

A 66-year-old male presented with dysarthria and right hemiparesis. Cerebral angiography at onset showed obliteration of the basilar artery and dilatation in the left vertebral artery. The patient's clinical symptoms were exaggerated and he was finally diagnosed to as suffering locked-in syndrome. Magnetic resonance imaging showed a brain stem infarction from the pons to the left middle cerebellar peduncle. We determined that the patient suffered dissection of the left vertebral artery at the basilar artery and treated, using the conservative therapy him of strict blood pressure control. A second angiography 13 days after onset showed recanalization of the basilar artery. At 29 days after onset, the patient fell into a coma with subarachnoid hemorrhage and acute hydrocephalus. Cerebral angiography revealed improvement in the irregularity and dilatation of the basilar artery, but the point of rupture could not be clearly identified. After performing proximal occlusion of the left vertebral artery by intravascular surgery, both right STA-SCA anastomosis and proximal occlusion of the right vertebral artery were carried out. Unfortunately, the patient died. Based on there data, it is appointed out that patients with a dissection of the vertebrobasilar artery must be followed up by serial angiography, and even if an angiographical improvement of the dissection is observed, the risk of subarachnoid hemorrhage still exists in patients suffering ischemic stroke.

Aged↗
PubMed2005

Cinnamophilin reduces oxidative damage and protects against transient focal cerebral ischemia in mice.

Acute neuroprotective effects of cinnamophilin (CINN; (8R, 8'S)-4, 4'-dihydroxy-3, 3'-dimethoxy-7-oxo-8, 8'-neolignan), a novel antioxidant and free radical scavenger, were studied in a mouse model of transient middle cerebral artery (MCA) occlusion. CINN was administered intraperitoneally either 15 min before (pretreatment) or 2 h after the onset of MCA occlusion (postischemic treatment). Relative to vehicle-treated controls, animals pretreated with CINN, at 20-80 mg/kg, had significant reductions in brain infarction by 33-46% and improvements in neurobehavioral outcome. Postischemic administration with CINN (80 mg/kg) also significantly reduced brain infarction by 43% and ameliorated neurobehavioral deficits. Additionally, CINN administration significantly attenuated in situ accumulation of superoxide anions (O2-) in the boundary zones of infarct at 4 h after reperfusion. Consequently, CINN-treated animals exhibited significantly decreased levels of oxidative damage, as assessed by immunopositive reactions for 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 4-hydroxynonenal (4-HNE), and the resultant inflammatory reactions at 24 h post-insult. It is concluded that CINN effectively reduced brain infarction and improved neurobehavioral outcome following a short-term recovery period after severe transient focal cerebral ischemia in mice. The finding of a decreased extent of reactive oxygen species and oxidative damage observed with CINN treatment highlights that its antioxidant and radical scavenging ability is contributory.

Animals↗
PubMed1993

Platelet aggregation inhibitors in neurology.

This literature review reports on secondary prevention of ischaemic stroke. The aim of secondary prevention is to protect patients who belong to a risk group from the occurrence of brain infarction. Symptomatic patients with a demonstrated carotid artery stenosis of 70% and more will most probably benefit from carotid endarterectomy if performed by a skilled surgeon in the absence of contraindications. Oral anticoagulant drugs play a minor role in the medical prevention of brain infarction. Antiplatelet drugs, however, have been in use for almost two decades and (meta-)analysis of clinical trials points to acetylsalicylic acid as a drug with a modest but certain contribution of about 15% in the endpoint reduction, even at lower dosages. The addition of dipyridamole to classic acetylsalicylic acid dose appears to increase the endpoint reduction to 30%. Neither dipyridamole nor sulfinpyrazone as monotherapy have been demonstrated to be efficacious in the secondary prevention of ischaemic stroke. Ticlopidine seems a promising alternative for acetylsalicylic acid in those patients who suffer adverse effects from acetylsalicylic acid. Ticlopidine itself, however, has a number of side-effects that limit its application. New clinical trials are under way in order to improve the efficacy of drug treatment in the secondary prevention of brain infarction.

Brain Ischemia↗