Cerebral vasculopathy in HIV infection revealed by transcranial Doppler: A pilot study.
(17/2638)
BACKGROUND AND PURPOSE: There is growing evidence for affection of cerebral vessels during human immunodeficiency virus (HIV) infection. We prospectively evaluated cerebrovascular reserve capacity (CRC) in HIV-seropositive patients by transcranial Doppler sonography (TCD) after systemic administration of acetazolamide. We hypothesized that a disturbed vasoreactivity would reflect the cerebral arteries' involvement in HIV infection. METHODS: We assessed the mean blood flow velocity (BFV) of the middle cerebral artery and its increase after intravenous administration of 1 g acetazolamide (CRC) in 31 HIV-infected individuals without symptoms of cerebrovascular disease (mean+/-SD age, 39+/-11 years). Stenotic or occlusive lesions of the large brain-supplying arteries were excluded by color-coded duplex and transcranial imaging. BFV and CRC were also measured in an age-matched group of 10 healthy control subjects. Patients were classified according to clinical, laboratory, and neurophysiological parameters. We also performed cerebral MRI (n=25) and rheumatological blood tests (n=26). RESULTS: Baseline BFV and CRC both were significantly reduced in HIV-infected patients as compared with control subjects (P<0.05, Student's t test). These findings did not correlate with duration of seropositivity, helper cell count, or other clinical, rheumatological, and neuroradiological findings. CONCLUSIONS: Our findings support the hypothesis of a cerebral vasculopathy etiologically associated with HIV infection. (+info)
Frontal bone windows for transcranial color-coded duplex sonography.
(18/2638)
BACKGROUND AND PURPOSE: The use of the conventional temporal bone window for transcranial color-coded duplex sonography (TCCS) often results in difficulties in obtaining angle-corrected flow velocity measurements of the A2 segment of the anterior cerebral artery, the posterior communicating artery, and the midline venous vasculature because of the unfavorable insonation angle. The same applies to B-mode imaging of the frontal parenchyma. However, transorbital TCCS raises problems with the insonation of the orbital lens. To overcome these drawbacks, we studied the feasibility of frontal bone windows for TCCS examinations. METHODS: In 75 healthy volunteers (mean age, 45.3+/-17.0 years; age range, 17 to 77 years), the circle of Willis and the venous midline vasculature were insonated through a lateral and paramedian frontal bone window. Insonation quality of parenchymal structures (B-mode) was graded on a 3-point scale depending on the visibility of typical parenchymal landmarks. In a similar manner, the quality of the color-/Doppler-mode imaging of the arteries of the circle of Willis and the internal cerebral veins was assessed. In 15 patients (mean age, 62.7+/-13.7 years; age range, 33 to 83 years), the color-/Doppler-mode imaging quality of the intracranial vessels before and after application of an ultrasound contrast-enhancing agent was compared. RESULTS: B-mode insonation quality was optimal to fair in 73.3% of cases using the lateral and in 52.0% of cases using the paramedian frontal bone window, with defined parenchymal structures used as reference. Insonation quality decreased in those older than 60 years. In those younger than 60 years, angle-corrected flow velocity measurements of the A2 segment of the anterior cerebral artery and the internal cerebral vein were possible in 73.6% and 60.0%, respectively. Contrast enhancement resulted in a highly significant improvement in the imaging quality of the intracranial vessels. CONCLUSIONS: The transfrontal bone windows offer new possibilities for TCCS examinations, although the insonation quality is inferior to the conventional temporal bone window in terms of failure of an acoustic window. This can be compensated for by application of an ultrasound contrast-enhancing agent. (+info)
Blockade of ATP-sensitive potassium channels in cerebral arterioles inhibits vasoconstriction from hypocapnic alkalosis in cats.
(19/2638)
BACKGROUND AND PURPOSE: Recent studies have shown that the cerebral arteriolar dilation from hypercapnic acidosis is blocked by agents which inhibit KATP channels. These findings suggested that this response is due to opening of KATP channels. Because the repose to CO2 is a continuum, with hypercapnic acidosis causing vasodilation and hypocapnic alkalosis causing vasoconstriction, it would be expected that the response to hypocapnic alkalosis would be due to closing of KATP channels. There are no studies of the effect of inhibition of KATP channels on the response to hypocapnic alkalosis. METHODS: We investigated the effect of 3 agents that in earlier studies were found to inhibit KATP channels--NG-nitro-L-arginine, hydroxylysine, and glyburide--on the cerebral arteriolar constriction caused by graded hypocapnia induced by hyperventilation in anesthetized cats equipped with cranial windows. RESULTS: Hypocapnic alkalosis caused dose-dependent vasoconstriction that was inhibited completely by each of the 3 inhibitors of KATP channels. The blockade induced by these agents was eliminated in the presence of topical L-lysine (5 micromol/L). CONCLUSIONS: The findings show that agents which inhibit ATP-sensitive potassium channels in cerebral arterioles inhibit the vasoconstriction from hypocapnic alkalosis. These and earlier results showing that inhibition of KATP channels inhibited dilation from hypercapnic acidosis demonstrate that the response to CO2 in cerebral arterioles is mediated by the opening and closing of KATP channels. (+info)
Amelioration of vasospasm after subarachnoid hemorrhage in transgenic mice overexpressing CuZn-superoxide dismutase.
(20/2638)
BACKGROUND AND PURPOSE: To clarify the effect of superoxide dismutase (SOD) on vasospasm after subarachnoid hemorrhage (SAH), we investigated sequential changes in arterial diameter after SAH in transgenic mice overexpressing CuZn-SOD (SOD-1). METHODS: SOD-transgenic mice and nontransgenic littermates (35 to 40 g) were subjected to SAH produced by endovascular perforation of left anterior cerebral artery. At 4 hours and 1, 3, 7, and 14 days after SAH, the mice were perfused with 10% formalin and consequently with a mixture of carbon black and 10% gelatin to cast all vessels. Vasospasm was evaluated by measuring the diameter of the left middle cerebral artery (MCA) with a microscope. RESULTS: In nontransgenic mice, the diameter of the MCA on day 3 after SAH (110.5+/-20.5 microm [mean+/-SD]; n=16) was significantly reduced compared with that without SAH (138.5+/-14.5 microm; n=12) (P<0.01). Moreover, on day 3 after SAH, the diameter of the MCA in SOD-transgenic mice (127. 9+/-20.2 microm; n=20) was significantly larger than that in nontransgenic mice (110.5+/-20.5 microm; n=16) (P<0.05). CONCLUSIONS: These results suggest that SOD is effective on the amelioration of vasospasm after SAH and that oxygen free radicals, particularly superoxide, play an important role in the pathogenesis of vasospasm after SAH. (+info)
Abnormal ductus venosus blood flow: a clue to umbilical cord complication.
(21/2638)
We report a case of umbilical cord complication causing, fetal hypoxemia and acidemia. At 30 weeks of gestation, the patient was referred because of slightly increased amniotic fluid volume and a non-reactive cardiotocogram. Biometry was appropriate for gestational age. Umbilical artery and fetal aortic Doppler findings were normal, whereas diastolic blood flow velocities in the middle cerebral artery were increased and the ductus venosus showed severely abnormal flow velocity waveforms with reversal of flow during atrial contraction. Since other reasons for fetal hypoxemia could be excluded, careful examination of the umbilical cord was performed. Traction of the hypercoiled umbilical cord due to its course around the fetal neck and shoulders was suspected. Cesarean section confirmed the sonographic findings and fetal blood gases revealed fetal acidemia. This case indicates that investigation of fetal venous blood flow may also help to identify fetal jeopardy due to reasons other than increased placental vascular resistance. (+info)
Intracranial arteries of human fetuses are more resistant to hypercholesterolemia-induced fatty streak formation than extracranial arteries.
(22/2638)
BACKGROUND: Atherosclerotic lesions in intracranial arteries occur later and are less extensive than in extracranial arteries. To investigate potential mechanisms responsible for this difference, in particular the atherogenic response to hypercholesterolemia and LDL oxidation, we compared the extent of fatty streak formation and the composition of these very early lesions in intracranial arteries of human fetuses from normocholesterolemic and hypercholesterolemic mothers with those in extracranial arteries. METHODS AND RESULTS: Lesions were quantified by computer-assisted image analysis of 30 oil red O-stained sections, each from the middle cerebral, basilar, and common carotid arteries and the abdominal aorta of human fetuses (spontaneous abortions and premature newborns who died within 12 hours of birth; both of fetal age 6.2+/-1.3 months) from 43 hypercholesterolemic mothers and 34 normocholesterolemic mothers. Macrophages, apolipoprotein B, and 2 epitopes of oxidized LDL in lesions were determined immunocytochemically. Activities of superoxide dismutase, catalase, and glutathione peroxidase in the arterial wall were also determined. Lesion numbers and sizes were dramatically greater in the abdominal aorta (area of the largest lesion per section: 66.5+/-10.9 x10(3) microm2) and the carotid (11. 6+/-5.3 x10(3) microm2) than in the basilar and middle cerebral artery (0.4+/-0.1 and 0.8+/-0.2 x10(3) microm2, respectively; P<0. 0001). Hypercholesterolemia resulted in a significant increase of lesion size in extracranial arteries but only a marginal increase in intracranial arteries. In analogy, hypercholesterolemia induced a much greater increase in the intimal presence of macrophages, apolipoprotein B, and oxidized LDL (oxidation-specific epitopes) in extracranial than in intracranial arteries. Immunocytochemistry did not indicate that lesions of intracranial arteries contain relatively less oxidized LDL than similar-size lesions of extracranial arteries. Activities of Mn-superoxide dismutase but not of Zn-superoxide dismutase, catalase, or glutathione peroxidase were significantly higher in both intracranial arteries. CONCLUSIONS: Exposure to hypercholesterolemia during fetal development results in extensive formation of fatty streaks in extracranial but not intracranial arteries. The fact that such a difference in lesion formation occurs in the absence of many other atherogenic risk factors found later in life suggests that differences in the atherogenic response to hypercholesterolemia are an important contributor to the slower onset of the disease in intracranial vessels in adults. Fetal arteries may allow elucidation of the mechanisms responsible, for example, better protection of intracranial arteries against free radical-mediated atherogenic processes. (+info)
Microangiopathy of the brain and retina with hearing loss in a 50 year old woman: extending the spectrum of Susac's syndrome.
(23/2638)
A 50 year old woman presented with a subacute onset of vertigo and diplopia followed by an encephalopathy with confusion, spasticity, ataxia, myoclonus, and multiple branch retinal arteriolar occlusions and unilateral sensorineural deafness. Brain biopsy confirmed multiple microinfarcts with no vasculitis. After the procedure she had a right iliofemoral deep vein thrombosis and was found to be heterozygous for the factor V Leiden mutation. She was treated with anticoagulants and made a marked recovery with no relapses 6 months after presentation. This case extends the age range at which Susac's syndrome can present, and raises the possibility that the condition may be associated with abnormalities of coagulation. (+info)
Factors influencing successful angiographic occlusion of aneurysms treated by coil embolization.
(24/2638)
BACKGROUND AND PURPOSE: Coil embolization of berry aneurysms is a relatively new treatment whose long-term efficacy has yet to be established. The purpose of this study was, first, to attempt to identify factors that might be important in predicting success both at the time of treatment and at the time of follow-up angiography, and, second, to study changes in the aneurysm between treatment and follow-up to determine the frequency of these changes. METHODS: The pretreatment, posttreatment, and follow-up angiograms of the first 63 aneurysms (in 58 patients) treated at our institution between June 1992 and April 1995 were analyzed, and the percentage of occlusion of each aneurysm was calculated. The size of any rest was noted for the posttreatment and follow-up angiograms. Treatment success was defined as a residue of less than 2 mm. Aneurysms were said to have changed if the percentage of occlusion had altered by more than 2.5% or if the difference in rest size was greater than 0.25 mm. Possible factors influencing primary and follow-up success rates were correlated against these calculations. RESULTS: Success rates at treatment and follow-up were 71% and 65%, respectively. No change occurred in 41% of aneurysms, and 20% had a decrease in size of the residue. Twenty-eight percent had coil compaction, and 11% had aneurysmal growth. Neck size was the only significant variable in primary treatment success. Success at follow-up correlated significantly with neck size, initial treatment success, vasospasm at the time of treatment, and clinical presentation. CONCLUSION: Best long-term angiographic results are obtained when the primary treatment is successful, when the aneurysm is small and narrow-necked, when the acutely ruptured aneurysm is treated within 15 days of ictus, and with anterior communicating and basilar-tip aneurysms. (+info)