Clinico-radiological correlation of magnetic resonance imaging findings in patients with idiopathic intracranial hypertension.

PURPOSE: Although several studies have reported imaging findings associated with idiopathic intracranial hypertension (IIH), less is known about the correlation between imaging findings and IIH-related symptoms or signs. Our study aimed to determine if clinical features of IIH are correlated with magnetic resonance imaging (MRI) features. METHODS: A retrospective chart review was conducted on consecutive patients presenting at the neuro-ophthalmology department over the last 15 years. All patients diagnosed with IIH were identified and those with available MRI were included in the final analysis. All MRI images were reviewed by a neuroradiologist blinded to the presenting symptoms and signs. Statistical analysis was performed to determine the correlation between the MRI findings with each clinical symptom or sign. RESULTS: Thirty-one out of 88 patients with the initial diagnosis of IIH had MRI available and were included in the study. Significant correlations were observed between colour vision and amount of perineural fluid around the optic nerve on MRI (r = - 0.382; p = 0.004), disc assessment and intraocular optic nerve protrusion (r = 0.364; p = 0.004), disc assessment and perineural fluid around the optic nerve (r = 0.276; p = 0.033) and disc assessment and venous sinus stenosis (r = 0.351; p = 0.009). CONCLUSION: Our study highlights correlations between imaging and clinical findings of IIH. MRI findings in IIH may be useful in ruling out ominous causes of intracranial pressure and risk stratifying ophthalmologic intervention and management of patients with headaches possibly due to IIH.

Thromboxane and neutrophil changes following intermittent claudication suggest ischaemia-reperfusion injury.

OBJECTIVES: It has been postulated that ischaemia-reperfusion occurs in intermittent claudication resulting in neutrophil activation and release of soluble mediators, increasing systemic vascular permeability and enhancing atherogenesis. METHODS: We measured neutrophil deformability, plasma thromboxane levels, and urinary microalbumin excretion in 30 male claudicants, and 10 age- and sex-matched controls, before and after exercise to maximum walking distance. Blood was taken from an antecubital vein. RESULTS: There was an increase in urinary microalbumin excretion after exercise in claudicants. Statistically significant increases in the median and 90th percentile transit times (markers of neutrophil deformability) for isolated neutrophils from blood drawn 5 min after exercise in the claudicants were observed with no change in control subjects. Plasma thromboxane concentrations in claudicants increased within 10 min post-exercise. Plasma concentrations in controls were significantly lower throughout the study period. In the claudicant group, a positive correlation between the percentage change in the median transit time for neutrophils, and the percentage change in plasma thromboxane at 60 min post-exercise was found. CONCLUSIONS: The results lend further support to the concept of ischaemia-reperfusion events in patients with intermittent claudication, leading to a systemic increase in vascular permeability as a result of endothelial injury or dysfunction (a crucial step in atherogenesis), associated with thromboxane production and neutrophil activation. We suggest that the above changes may contribute to the increased mortality seen in such patients.

Generalized vascular permeability and pulmonary function in patients following serious trauma.

It has been suggested that the adult respiratory distress syndrome (ARDS) is a manifestation of a generalized vascular permeability defect. Low-level urinary albumin excretion reflects changes in systemic vascular permeability in a variety of acute inflammatory conditions including trauma. To test the hypothesis that impaired pulmonary function is associated with increased systemic vascular permeability, 44 trauma patients with Injury Severity Scores (ISS) ranging from 9 to 75 were studied over 3 days. Urinary albumin was measured from admission and expressed as the albumin/creatinine ratio (ACR). In 24 mechanically ventilated patients mean inspired oxygen/fraction (FIO2) and mean arterial oxygen tension (PO2) were used to calculate the PO2/FIO2 ratio. For each study day patients were divided into group I, mean FIO2 > 0.5; group II, mean FIO2 < 0.5; and group III, those breathing spontaneously. During the first posttrauma period the log ACR and the PO2/FIO2 ratio were inversely related (r = -0.712; p < 0.001), and the log ACR predicted PO2/FIO2 independent of ISS (p = 0.001). The log mean ACR (SD) for groups I and III were 34.0 (5.6) and 8.7 (2.9) mg/mmol, respectively (Mann Whitney p = 0.013). Following trauma, pulmonary dysfunction is associated with increased vascular permeability in remote organs.

Pharmacological reduction of the systemically damaging effects of local ischaemia.

Many patients with intermittent claudication are encouraged to exercise. However, transient exercise-induced muscle ischaemia results in systemic vascular endothelial injury associated with increased vascular permeability manifest as an increase in urinary albumin excretion. Repetitive systemic vascular endothelial injury leads to accelerated atherogenesis and may explain the high cardiovascular mortality rate of claudicants. Oxpentifylline, a haemorheological agent, has recently been shown to prevent vascular endothelial injury in animal models. A double-blind, placebo-controlled, cross-over trial was undertaken to determine the effect of oxpentifylline on exercise-induced systemic vascular endothelial injury in 20 claudicants. Urinary albumin, expressed as a creatinine ratio (ACR), was measured before and 1 and 2 hours after standardised exercise following 1 week treatment with either active drug or placebo. Oxpentifylline reduced the median (range) 1 hour post exercise increase in ACR from 0.35 (-0.46-12.72) to 0.02 (-6.00-14.10) mg/mmol. (p = 0.030, z = 2.2 Wilcoxon rank sign test). These results confirm that local ischaemia is associated with a potentially deleterious systemic effect and that it may be possible to attenuate this pharmacologically. The clinical significance of this is yet to be determined.

Dermatomyositis associated with Lyme disease: case report and review of Lyme myositis.

Myositis due to the etiologic agent of Lyme disease, Borrelia burgdorferi, has been reported nine times in the English-language literature; there has been but a single report of exacerbation of dermatomyositis due to B. burgdorferi in a patient with known dermatomyositis. Multiple infectious agents, but not B. burgdorferi, have been hypothesized to trigger dermatomyositis. We report the first case of dermatomyositis that appears to have been triggered by B. burgdorferi. This case involved an individual from Westchester County, NY, who presented with skin lesions suggestive of erythema migrans and who was seropositive for Lyme disease. He soon developed a clinical syndrome suggestive of dermatomyositis: periorbital edema, dysphagia, proximal muscle weakness, and a markedly elevated level of creatine phosphokinase. We also review the clinical presentation and response to treatment of patients with Lyme myositis.

Microproteinuria predicts the severity of systemic effects of reperfusion injury following infrarenal aortic aneurysm surgery.

Noncardiogenic pulmonary dysfunction can be demonstrated in all patients following elective aortic aneurysm repair and is a cause of postoperative morbidity. Aortic clamping and reperfusion initiate a systemic inflammatory response producing endothelial damage and increases in vascular permeability. In the lung this is manifest as pulmonary edema and in the kidney as detectable increases in urinary protein excretion (microproteinuria). Immunoassay of low-level protein excretion appears to provide an index of the systemic effects of local reperfusion injury and may allow early prediction of complications such as pulmonary edema. Hourly urinary albumin and IgG excretion was measured in 40 patients undergoing infrarenal aortic aneurysm repair and expressed as ratios to urinary creatinine (albumin/creatinine ratio [ACR] and IgG/creatinine ratio [IgGCR]). These were compared to clinical outcome. Pulmonary dysfunction was assessed according to PaO2:FiO2 ratios and chest radiography. Within 180 minutes of beginning surgery all patients had significant increases in ACR and IgGCR. Ten patients who manifested respiratory dysfunction had significantly higher ACRs at 4 hours (median 84.8, 95% confidence intervals, range 47.7 to 136) than patients who made uneventful recoveries (median 16.6, 95% confidence intervals, range 7.9 to 31.7). IgGCR increases paralleled that of ACRs. Differences persisted for 24 hours. Urinary protein excretion rises rapidly during aortic surgery. The degree of increase appears to predict development of pulmonary dysfunction. This simple test may provide a rational basis for evaluation of therapeutic modalities to limit reperfusion injury in these patients.