Magnetic resonance neurography: magnetic resonance imaging of peripheral nerves.

With advances in modern MR imaging, direct MR visualization of many peripheral nerves is now possible. MR nerve imaging can detect and delineate the extent of neural tumors, demonstrate nerve continuity in cases of traumatic injury, and demonstrate abnormal enlargement and abnormal signal in diseased peripheral nerves. This ability to image peripheral nerves has the potential to dramatically change the diagnosis and treatment of peripheral nerve disease. This article describes the techniques for peripheral nerve imaging and provides a brief overview of a broad spectrum of peripheral nerve abnormalities.

Adenosine-induced ventricular asystole to induce transient profound systemic hypotension in patients undergoing endovascular therapy. Dose-response characteristics.

BACKGROUND: Adenosine-induced asystole has been used to induce transient systemic hypotension for various vascular procedures. Dose-response characteristics of adenosine-induced ventricular asystole have not been determined. METHODS: During endovascular embolization of cerebral arteriovenous malformations, the authors performed a series of adenosine test injections to establish a dose-response relation in each patient. After an interval of 3-10 min, the dose was escalated by 10-20 mg for each injection to achieve an end point of 20-30 s of stable mean arterial pressure (MAP) reduction to 25-30 mmHg. All patients received constant infusion of nitroprusside (approximately 1 microgram. kg-1. min-1) throughout the procedure. RESULTS: The authors studied four adult patients (age, 22-44 yr; two patients had two separate procedures) and one pediatric patient (age, 4 yr). Twenty-three adenosine injections resulted in measurable asystole. The adenosine dose was 0. 98 +/- 0.40 mg/kg (mean +/- SD), and the dose range was 0.24-1.76 mg/kg (6-90 mg). The duration of asystole, MAP < 30 mmHg, and MAP < 50 mmHg, were 8 +/- 3 s, 18 +/- 12 s, and 50 +/- 29 s, respectively. The minimum MAP and the MAP for the first 20 s were 16 +/- 3 mmHg and 30 +/- 9 mmHg, respectively. There was a linear relation between adenosine dose and the duration of hypotension with MAP < 30 mmHg and MAP < 50 mmHg. CONCLUSIONS: In the dose range studied, a series of adenosine test injections can be used to determine optimal adenosine dose for induction of transient profound hypotension.

Incident hemorrhage risk of brain arteriovenous malformations located in the arterial borderzones.

BACKGROUND AND PURPOSE: We sought to assess the relative risk of hemorrhagic presentation of brain arteriovenous malformations (AVMs) located in the arterial borderzone territories. METHODS: The 464 consecutive, prospectively enrolled patients from the New York AVM Databank were analyzed. AVM borderzone location was coded positive when the malformation was supplied by branches of at least 2 of the major circle of Willis arteries (anterior, middle, and/or posterior cerebral arteries). AVMs fed by branches of only 1 major pial or any other single artery served as a comparison group. Clinical presentation (diagnostic event) was categorized as (1) intracranial hemorrhage, proven by brain imaging, or (2) seizure, focal neurological deficit, headache, or other event with no signs of AVM hemorrhage on brain imaging. RESULTS: In 48% (n=222) of the patients, AVMs were located in the arterial borderzone territories; in 52% (n=242) a non-borderzone location was found. Hemorrhage was the presenting symptom in 44% (n=205); 28% (n=132) presented with seizures, 11% (n=52) with headaches, 7% (n=34) with a neurological deficit, and 9% (n=41) with other or no AVM-related symptoms. The frequency of incident AVM hemorrhage was significantly lower in borderzone AVMs (27%, n=61) than in non-borderzone malformations (60%, n=144; P:<0.001). This difference remained significant in a multivariate model controlling for age, sex, AVM size, deep venous drainage, and presence of aneurysms (odds ratio, 0.4; 95% CI, 0.25 to 0.66). CONCLUSIONS: Our findings suggest that borderzone location is an independent determinant for a lower risk of AVM hemorrhage at initial presentation.

Intracarotid infusion of the nitric oxide synthase inhibitor, L-NMMA, modestly decreases cerebral blood flow in human subjects.

BACKGROUND: The authors hypothesized that if nitric oxide (NO) was a determinant of background cerebrovascular tone, intracarotid infusion of NG-monomethyl-L-arginine (L-NMMA), a NO synthase (NOS) inhibitor, would decrease cerebral blood flow (CBF) and intracarotid L-arginine would reverse its effect. METHODS: In angiographically normal cerebral hemispheres, after the initial dose-escalation studies (protocol 1), the authors determined the effect of intracarotid L-NMMA (50 mg/min for 5 min) on CBF and mean arterial pressure (MAP) over time (protocol 2). Changes in CBF and MAP were then determined at baseline, during L-NMMA infusion, and after L-NMMA during L-arginine infusion (protocol 3). To investigate effects of higher arterial blood concentrations of L-NMMA, changes in CBF and MAP were assessed at baseline and after a bolus dose of L-NMMA (250 mg/1 min), and vascular reactivity was tested by intracarotid verapamil (1 mg/min, protocol 4). CBF changes were also assessed during induced hypertension with intravenous phenylephrine (protocol 5). RESULTS: Infusion of L-NMMA (50 mg/min for 5 min, n = 7, protocol 2) increased MAP by 17% (86 +/- 8 to 100 +/- 11 mmHg; P < 0.0001) and decreased CBF by 20% (45 +/- 8 to 36 +/- 6 ml. 100 g-1. min-1; P < 0.005) for 10 min. Intracarotid l-arginine infusion after L-NMMA (protocol 3) reversed the effect of L-NMMA. Bolus L-NMMA (protocol 4) increased MAP by 20% (80 +/- 11 to 96+/-13 mmHg; P< 0.005), but there was no significant decrease in CBF. Intracarotid verapamil increased CBF by 41% (44+/- 8 to 62 +/- 9 ml. 100 g-1. min-1; P< 0.005). Phenylephrine-induced hypertension increased MAP by 20% (79 +/- 9 to 95 +/- 6 mmHg; P = 0.001) but did not affect CBF. CONCLUSIONS: The results suggest that intracarotid L-NMMA modestly decreases CBF, and the background tone of cerebral resistance vessels may be relatively insensitive to NOS inhibition by the intraarterial route.

Complex right hemisphere developmental venous anomaly associated with multiple facial hemangiomas. Case report.

Complex developmental venous anomalies (DVAs) represent variations of normal cerebral venous drainage and consist of dilation of the superficial and/or deep venous system. These rare anomalies can occur unilaterally or bilaterally, supratentorially or infratentorially, focally or they can affect the entire hemisphere. Some DVAs are associated with cervicofacial venous malformations or facial lymphatic malformations. Anomalies of this type are generally clinically silent, and cerebral dysfunction is usually absent. Symptoms, when they occur, are most commonly headache or mild seizure disorders. The angiographic findings are striking, with well-formed but enlarged transcerebral medullary and deep and/or superficial cortical veins. Opacification of these venous structures occurs within the same time frame as a normal angiographic venous phase. The authors report the case of a 33-year-old man in whom a large inoperable arteriovenous malformation had been previously diagnosed and who presented with seizures. Repeated magnetic resonance imaging and angiography demonstrated abnormally dilated transcerebral, superficial, and deep venous structures involving the entire right hemisphere with no identifiable nidus. Additionally, multiple bilateral benign facial hemangiomas were present in this patient. It is important to recognize this rare venous appearance as a developmental variant and not mistake it for an arteriovenous malformation or a partially thrombosed vein of Galen malformation. Because these venous anomalies are extreme variants of the normal venous system, hemorrhage rarely, if ever, occurs and the patient can be reassured that no interventional or surgical therapy is necessary or warranted.

MR neurography. MR imaging of peripheral nerves.

Recent advances in MR imaging coupled with specially designed phased-array surface coils are revolutionizing imaging of the peripheral nervous system. Direct visualization of normal-sized major peripheral nerves within the body is now possible. This article describes the appearance of normal peripheral nerves together with imaging characteristics of various types of nerve pathology including traumatic injury, compressive syndromes, and neural tumors. Imaging of the brachial plexus, lumbosacral plexus, carpal tunnel, cubital tunnel, and cervical nerves is illustrated and discussed. MR neurography techniques permit imaging detection of peripheral nervous system pathology that in some cases allow earlier and more accurate diagnosis. It is believed that this will ultimately lead to improved understanding of peripheral nerve pathophysiology that will, in turn, lead to improved treatment.

Intestinal immunisation with Escherichia coli protects rats against Escherichia coli induced cholangitis.

BACKGROUND: Cholangitis, an infection of the biliary tract, is most commonly caused by Gram negative bacteria, particularly Escherichia coli. Factors governing the severity of cholangitis, including the role of biliary IgA, are poorly understood. AIMS: The aim of this work was to find out if biliary IgA directed against E coli protects rats against hepatobiliary infection with E coli. SUBJECTS: Male Sprague-Dawley rats weighing 270-350 grams were used in all of the experiments. METHODS: At laparotomy, rats were immunised by injecting killed E coli or normal saline (controls) into Peyer's patches. With or without subsequent antigenic boosting (by oral administration of killed E coli), bile was collected at a second laparotomy, and rats were infected by introducing viable E coli into the bile duct. Production of IgA anti-E coli antibody was measured by enzyme linked immunosorbent assay of bile, and the presence of hepatobiliary infection was determined by quantitative culture of liver homogenates. RESULTS: Systemic infection was present in six of 12 control rats and in one of 24 immunised rats (p = 0.005) after death. There was an inverse correlation between immunisation and E coli colony counts in cultured liver homogenates (p = 0.024). CONCLUSION: The findings suggest that biliary IgA directed against E coli protected rats against hepatobiliary E coli infection and systemic sepsis.

Heat ablation of the normal gallbladder in pigs.

PURPOSE: The safety and efficacy of ablating gallbladder mucosa was investigated with a percutaneously placed heater catheter in an animal study. MATERIALS AND METHODS: The study was performed in three stages with 39 pigs. In stage 1 (15 heat-treated animals, one control), the configuration of the heater catheter was progressively improved and the temperature settings for stage 2 were defined. In stage 2 (11 heat-treated animals, four controls), the predetermined settings were used with mechanical mixing and cystic duct ligation to test for safety and efficacy. In stage 3 (eight animals), prior heat ablation of the cystic duct was added to reduce epithelial regeneration. RESULTS: Gallbladder ablation was achieved at temperatures below 60 degrees C. Mechanical mixing of the intraluminal contents was essential for even heat distribution for ablation and to reduce the incidence of adjacent organ damage. Thermal injury to adjacent organs occurred when gallbladder ablation temperature exceeded 54 degrees C and serosal temperatures of adjacent organs exceeded 43 degrees C. Thermal ablation at 54 degrees C for 35 minutes was completely successful in 25%, partially successful in 50%, and failed in 25% of animals. Cystic duct ablation improved overall results and appears vital in removing duct epithelium as a source for regeneration of the mucosal lining. CONCLUSION: Defunctionalization of the retained gallbladder is potentially achievable with use of thermal techniques, but the thermal range between complete gallbladder ablation and adjacent organ injury is narrow.