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(1/30) Immediate surgery reduces mortality in deeply comatose patients with spontaneous cerebellar hemorrhage.

Cerebellar hemorrhage is regarded as a neurosurgical emergency. However, patients with deteriorating consciousness are very likely to die irrespective of the choice of therapy, and it is not clear if surgical intervention can benefit patients in a deeply comatose state. We reviewed 20 patients with a Glasgow Coma Scale score of 3 at admission to ascertain the salvage rate and determine the prognostic factors. Four patients who were managed conservatively died within 2 days. Sixteen patients underwent decompressive suboccipital craniectomy and hematoma evacuation. At discharge, three patients were moderately disabled, three were severely disabled, four were persistently vegetative, and six had died. The overall mortality was 50%. The mean interval between the onset of symptoms and the operation was 1.67 +/- 0.29 hours in patients with favorable outcome, and significantly longer at 2.42 +/- 0.49 hours in patients with an unfavorable outcome (p = 0.025). Immediate evacuation of the hematoma reduces morbidity and mortality even in deeply comatose patients, especially if the time interval between the onset and surgery is within 2 hours.  (+info)

(2/30) Relationship between stroke and asymptomatic minute hemorrhages in hypertensive patients.

Asymptomatic small hemorrhages were identified in hypertensive patients by T2*-weighted gradient echo magnetic resonance (MR) imaging to investigate the relationship between hypertensive intracerebral hemorrhage and asymptomatic minute hemorrhages. Forty-eight patients with hypertensive intracerebral hemorrhage or cerebral infarction with hypertension (these diseases were defined as stroke) were treated in National Defense Medical College from April 1998 to February 2000. All patients had no past history of stroke or head injury, underwent MR imaging within 6 months of the stroke attack, were aged from 40 to 80 years, and had no diagnosis of aneurysm, angioma, or moyamoya disease. Patients were divided into the infarction group and hemorrhage group. All foci over 2 mm in size appearing as hypointense on T2*-weighted MR imaging and unrelated to stroke areas were defined as minute hemorrhages. There were no significant differences between the two groups with respect to sex, age, and history of diabetes mellitus. The incidence of minute hemorrhages in the hemorrhage group (21/26) was greater than in the infarction group (9/22, p < 0.01). The incidence of minute hemorrhages in the basal ganglia (18/26) was greater in the hemorrhage group than in the infarction group (4/22, p < 0.001). Symptomatic intracerebral hemorrhage may be preceded by asymptomatic minute hemorrhage.  (+info)

(3/30) Endogenous interleukin-10 is required for prevention of a hyperinflammatory intracerebral immune response in Listeria monocytogenes meningoencephalitis.

To analyze the role of interleukin-10 (IL-10) in bacterial cerebral infections, we studied cerebral listeriosis in IL-10-deficient (IL-10(-/-)) and wild-type (WT) mice, the latter of which express high levels of IL-10 in both primary and secondary cerebral listeriosis. IL-10(-/-) mice succumbed to primary as well as secondary listeriosis, whereas WT mice were significantly protected from secondary listeriosis by prior intraperitoneal immunization with Listeria monocytogenes. Meningoencephalitis developed in both strains; however, in IL-10(-/-) mice the inflammation was more severe and associated with increased brain edema and multiple intracerebral hemorrhages. IL-10(-/-) mice recruited significantly increased numbers of leukocytes, in particular granulocytes, to the brain, and the intracerebral cytokine (tumor necrosis factor, IL-1, IL-12, gamma interferon, and inducible nitric oxide synthase) and chemokine (crg2/IP-10, RANTES, MuMig, macrophage inflammatory protein 1alpha [MIP-1alpha], and MIP-1beta) transcription was enhanced compared to that in WT mice. Despite this prominent hyperinflammation, the frequencies of intracerebral L. monocytogenes-specific CD8(+) T cells were reduced and the intracerebral bacterial load was not reduced in IL-10(-/-) mice compared to WT mice. Following intraperitoneal infection, IL-10(-/-) mice exhibited hepatic hyperinflammation without better bacterial clearance; however, in contrast to the mice with cerebral listeriosis, they did not succumb, illustrating that intrinsic factors of the target organ have a strong impact on the course and outcome of the infection.  (+info)

(4/30) Simultaneous occurrence of subarachnoid hemorrhage due to ruptured aneurysm and remote hypertensive intracerebral hemorrhage: case report.

Simultaneous occurrence of aneurysmal subarachnoid hemorrhage (SAH) and hypertensive intracerebral hemorrhage (ICH) is very rare and only two cases have been previously reported in the literatures. We present a case of 68-yr-old man with a history of untreated hypertension, who suffered from sudden onset of headache followed by right hemiparesis. Computed tomographic (CT) scan revealed SAH in the basal cistern and remote ICH at the left putamen. Cerebral angiography showed a saccular aneurysm at the anterior communicating artery. No other vascular anomaly could be found at left putaminal area. Nine days after the ictal attack of SAH, the neck of aneurysm was clipped via the left frontotemporal craniotomy. Because of the ICH at the left frontal lobe and intraventricular hematoma on postoperative CT, we performed hematoma removal and external ventricular drainage 3 hours after the first operation. Postoperative neurological status had been improved to be drowsy and he was discharged in a severely disabled state 4 weeks after surgery. We suggest that the rupture of aneurysm possibly caused a rapid increase in blood pressure and subsequently resulted in hypertensive ICH.  (+info)

(5/30) Stereotactic fibrinolysis of spontaneous intracerebral hematoma using infusion of recombinant tissue plasminogen activator.

PURPOSE: The authors present a prospective study on 10 patients with stereotactic infusion of tissue plasminogen activator (rtPA) intraparenchimal hemorrhage. METHODS: Between 1999 and 2000, 10 patients with deep seated hematomas in the basal ganglia were selected for stereotactic infusion of rtPA and spontaneous clot drainage. RESULTS: All cases had about 80% reduction of the hematoma volume in the CT scan at the third day. The intracranial pressure was normalized by the third day too. There were no local or systemic complications with the use of this thrombolytic. The results were shown by the Glasgow Outcome Scale with six patients in V, three in IV and one in III after 3 months. CONCLUSION: Early treatment and drainage with minimally invasive neurosurgery, can make these patients with deep-seated hematomas recover the consciousness and they can be rehabilitated earlier avoiding secondary complications.  (+info)

(6/30) Clinical and radiographic features of lobar cerebral hemorrhage: hypertensive versus non-hypertensive cases.

OBJECTIVES: The underlying cause of lobar intracerebral hemorrhage (ICH) is often difficult to determine, since these vascular abnormalities are not necessarily visualized in radiographic studies. We sought to determine the clinical features of hypertensive and nonhypertensive lobar ICH, and further predict the presence or absence of vascular abnormalities in terms of clinical features and radiographic abnormalities. PATIENTS AND METHODS: Eighty-one patients with lobar ICH were retrospectively assigned to either hypertensive or non-hypertensive groups based on their blood pressure levels during the chronic phase or a history of antihypertensive medication. The clinical and radiographic features of these two groups were compared. RESULTS: Forty-nine patients (60%) were hypertensive, and the other thirty-two (40%) were non-hypertensive. In the non-hypertensive group, amyloid angiopathy (n = 6), aneurysms (n = 5), arteriovenous malformation (n = 4), use of anticoagulants (n = 2), liver cirrhosis (n = 2) and thrombasthenia (n = 1) were found as underlying causes. There were no significant differences between these two groups in the frequencies of stroke risk factors except for hypertension, clinical features and initial neurological findings. On the contrary, subarachnoid extension of the hematoma on CT was significantly more frequent in the non-hypertensive lobar ICH group than in the hypertensive group (p < 0.001). The patients with subarachnoid extension were more likely to have vascular abnormality than those without subarachnoid extension (p < 0.01). CONCLUSION: Subarachnoid extension of the hematoma on CT strongly indicates a non-hypertensive cause, and more specifically, it suggests lobar ICH caused by vascular abnormalities.  (+info)

(7/30) Effect of untreated hypertension on hemorrhagic stroke.

BACKGROUND AND PURPOSE: Stroke is the third leading cause of death and the leading cause of disability in the United States. Intracerebral hemorrhage and subarachnoid hemorrhage represent approximately 20% of all stroke cases and have a mortality rate of 40% to 50%. Hypertension is an important risk factor for these subtypes of stroke. We sought to determine whether untreated hypertension carries a different risk from treated hypertension for hemorrhagic stroke. METHODS: Cases of hemorrhagic stroke in the greater Cincinnati region were identified by screening all area hospital emergency rooms, radiology reports, and International Classification of Diseases 9 codes. Medical records were reviewed for risk factors and medication use. Cases of hemorrhagic stroke were approached for enrollment into the genetic sampling and interview arm. If subjects agreed, the case was matched by age, race, and gender to population-based controls. RESULTS: Between May 1997 and December 2002, we recruited 549 cases of hemorrhagic stroke, of which 322 were intracerebral hemorrhage and 227 were subarachnoid hemorrhage. Untreated hypertension was found to be a significant risk factor for hemorrhagic stroke (odds ratio [OR]=3.5 [2.3 to 5.2]; P<0.0001) as was treated hypertension (OR=1.4 [1.0 to 1.9]; P=0.03). Insurance status of "self-pay" or Medicaid was a significant risk factor for untreated hypertension (OR=2.7 [1.6 to 4.4]). We estimate that 17% to 28% of hemorrhagic strokes among hypertensive patients would have been prevented if they had been on hypertension treatment. CONCLUSIONS: Untreated hypertension is highly prevalent and an important risk factor for hemorrhagic stroke. We estimate that among hypertensive subjects, approximately one fourth of hemorrhagic strokes would be prevented if all hypertensive subjects received treatment.  (+info)

(8/30) Study of cerebral vascular structures in hypertensive intracerebral haemorrhage.

AIMS: The study was performed in order to assess the alterations of extra-parenchymal and intraparenchymal vascular structures in 82 hypertensive patients suspected of primary intraparenchymal hematoma, which died and were autopsied in order to confirm the diagnosis. MATERIAL AND METHODS: The studied material consisted of nervous tissue situated near and distant from the haemorrhagic lesion. The specimens of nervous tissue were processed by the classical histological technique and stained with the usual stainings and with immunohistochemical stains for basement membranes and endothelial cells. RESULTS: Extra-parenchymal arteries showed classic lesions of atherosclerosis. Atheromatous lesions were of all types, even the extension towards the media being encountered a complication with thrombosis. At the level of the intraparenchymal blood vessels, the spectrum of the lesions due to arterial hypertension included all steps of vascular wall degeneration, from hypertrophy of smooth muscle layer to complete hyalinization of arterial wall, but with a focal irregular distribution, not related with the proximity of haemorrhagic focus. High arterial blood pressure also influenced the capillary walls which showed focal or circumferential thickening due to the densification of the type IV collagen material from the basement membrane structure. The CD34 immunostaining showed that endothelial cells kept their structural integrity. CONCLUSIONS: The sequence of degenerative lesions of the cerebral vascular wall culminates with the hyalinization of excessive fibrillar material form arteriolar wall or from basement membranes. Hyalin material is weakening the wall resistance to the stress determined by the high values of blood pressure in hypertension, and, correlated with a minimal resistance of the surrounding cerebral parenchyma, can explain why the cerebral parenchyma is the only tissue in which blood pressure variations can determinate vascular rupture and cerebral haemorrhage. The more adequate term for describing the vascular wall changes seems to be sclerosis (arteriolar and even capillary) with hyalinosis.  (+info)