Blood pressure fluctuations in posterior reversible encephalopathy syndrome.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) can be a consequence of hypertensive crisis and is often associated with rapid fluctuations in blood pressure (BP). However, the role of these BP changes in the pathogenesis of PRES has not been formally studied. Our objective was to analyze the relationship between BP fluctuations and the occurrence of PRES. METHODS: We identified consecutive patients who developed PRES in the hospital and compared them with randomly selected controls matched for age, gender, and history of hypertension (HTN). Systolic BP (SBP) and diastolic BP (DBP) were collected at 2-hour intervals over a 48-hour window before the onset of PRES symptoms. A profile of changes in the values of SBP, DBP, mean arterial pressure (MAP), and pulse pressure (PP) over the 48-hour window was summarized for each individual by calculating a single number (M value) using the approach by Service et al. Comparisons of these summary numbers between the 2 groups (cases and controls) were made with the Wilcoxon signed rank test because of the smaller sample size and paired nature of the data. All tests were 2-sided, and P < .05 was considered statistically significant. RESULTS: We analyzed the BP profiles in 25 cases of PRES and 25 controls. The median age of PRES patients was 54 years (range 31-72). Fourteen of them (56%) had a history of HTN. Hypertensive encephalopathy was considered the underlying cause of PRES in 13 patients (52%). At the time of the first symptoms of PRES, the mean SBP was 182 ± 20 mm Hg (range 218-145), DBP 95 ± 16 mm Hg (range 134-62), MAP 124 ± 15 (range 152-93), and PP 87 ± 18 (range 123-46). While BP was higher in PRES cases, the severity of HTN was variable and BP fluctuations were not significantly more common than in controls (P = .38 for SBP, .79 for DBP, .25 for MAP, and .73 for PP, respectively). CONCLUSIONS: Although acute HTN is frequent in patients with PRES, BP fluctuations do not appear to be more common in hospitalized patients who develop PRES compared with controls matched for age and history of HTN. Other predisposing factors must therefore contribute to the development of PRES.

Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings.

OBJECTIVE: To identify and define clinical associations and radiologic findings of posterior reversible encephalopathy syndrome (PRES). PATIENTS AND METHODS: Patients prospectively diagnosed as having PRES from October 1, 2005, through April 30, 2009, were pooled with retrospectively identified patients admitted from August 1, 1999, through September 30, 2005. We performed a detailed review of clinical information, including demographics, presenting symptoms, medical history, and risk factors. All patients underwent computed tomography of the brain or magnetic resonance imaging. Findings on magnetic resonance imaging were analyzed independently by 2 neuroradiologists. RESULTS: We identified 120 cases of PRES in 113 patients (mean age, 48 years). Mean peak systolic blood pressure was 199 mm Hg (minimum-maximum, 160-268 mm Hg), and mean peak diastolic blood pressure was 109 mm Hg (minimum-maximum, 60-144 mm Hg). Etiologies of PRES included hypertension (n=69 [61%]), cytotoxic medications (n=21 [19%]), sepsis (n=8 [7%]), preeclampsia or eclampsia (n=7 [6%]), and multiple organ dysfunction (n=1 [1%]). Autoimmune disease was present in 51 patients (45%). Clinical presentations included seizures (n=84 [74%]), encephalopathy (n=32 [28%]), headache (n=29 [26%]), and visual disturbances (n=23 [20%]). In the 115 cases (109 patients) for which magnetic resonance imaging findings were available, the parieto-occipital regions were the most commonly involved (n=108 [94%]), followed by the frontal lobe (n=88 [77%]), temporal lobe (n=74 [64%]), and cerebellum (n=61 [53%]). Cerebellar involvement was significantly more frequent in patients with a history of autoimmunity (P=.008), and patients with sepsis were more likely to have cortical involvement (P<.001). CONCLUSION: A substantial proportion of patients with PRES have underlying autoimmune conditions that may support endothelial dysfunction as a pathophysiologic mechanism. On brain imaging, the location and severity of vasogenic edema were mostly similar for the different clinical subgroups.

Super-selective intra-arterial magnesium sulfate in combination with nicardipine for the treatment of cerebral vasospasm in patients with subarachnoid hemorrhage.

OBJECTIVES: To determine the safety and tolerability of super-selective intra-arterial magnesium sulfate in combination with intra-arterial nicardipine in patients with cerebral vasospasm after subarachnoid hemorrhage. METHODS: Patients were treated in a prospective protocol at two teaching medical centers. Emergent cerebral angiography was performed if there was either clinical, ultrasound, and/or computed tomographic (CT) perfusion deficits suggestive of cerebral vasospasm. Intra-arterial magnesium sulfate (0.25-1 g) was administered via a microcatheter in the affected vessels in combination with nicardipine (2.5-20.0 mg). Mean arterial pressures (MAP) and intracranial pressures (ICP) were monitored during the infusion. Immediate and sustained angiographic and clinical improvement was determined from post-treatment angiograms and clinical follow-up. Angiographic and clinical outcomes were compared to two published case series that has used nicardipine alone. RESULTS: A total of 58 vessels were treated in 14 patients (mean age 42 years; 11 women) with acute subarachnoid hemorrhage. The treatment was either intra-arterial nicardipine and magnesium sulfate alone or in conjunction with primary angioplasty. Forty vessels (69%) had immediate angiographic improvement with intra-arterial nicardipine and magnesium sulfate alone and 18 vessels (31%) required concomitant balloon angioplasty with complete reversal of the vasospasm. Retreatment was required in 13 vessels (22%) and the median time for retreatment was 2 days (range 1-13 days). Nicardipine treatment resulted in the reduction of MAP (12.3 mmHg, standard error [SE] 1.34, P-value <0.0001) without any significant change in ICP. Magnesium sulfate infusion was not associated with change in MAP or ICP. Among 31 procedures, immediate neurological improvement was observed in 22 (71%) procedures. In 12 (86%) patients, there were no infarctions in the follow-up CT scan acquired between 24 and 48 h. No statistical significant difference was observed in angiographic and clinical outcome of patients treated with the combination therapy in comparison with historical controls treated with nicardipine alone. CONCLUSION: Administration of intra-arterial magnesium sulfate in combination with nicardipine was well tolerated in patients with subarachnoid hemorrhage and cerebral vasospasm without a significant change in MAP and ICP. The efficacy of this combination therapy should be evaluated in a larger, controlled setting.

Posterior reversible encephalopathy syndrome: incidence of atypical regions of involvement and imaging findings.

OBJECTIVE: Posterior reversible encephalopathy syndrome (PRES) is classically characterized as symmetric parietooccipital edema but may occur in other distributions with varying imaging appearances. This study determines the incidence of atypical and typical regions of involvement and unusual imaging manifestations. MATERIALS AND METHODS: Seventy-six patients were eventually included as having confirmed PRES from 111 initially suspected cases, per imaging and clinical follow-up. Two neuroradiologists retrospectively reviewed each MR image. Standard sequences were unenhanced FLAIR and T1- and T2-weighted images in all patients, with diffusion-weighted imaging (n = 75) and contrast-enhanced T1-weighted imaging (n = 69) in most. The regions involved were recorded on the basis of FLAIR findings, and the presence of atypical imaging findings (contrast enhancement, restricted diffusion, hemorrhage) was correlated with the severity (extent) of hyperintensity or mass effect on FLAIR. RESULTS: The incidence of regions of involvement was parietooccipital, 98.7%; posterior frontal, 78.9%; temporal, 68.4%; thalamus, 30.3%; cerebellum, 34.2%; brainstem, 18.4%; and basal ganglia, 11.8%. The incidence of less common manifestations was enhancement, 37.7%; restricted diffusion, 17.3%; hemorrhage, 17.1%; and a newly described unilateral variant, 2.6%. Poor correlation was found between edema severity and enhancement (r = 0.072), restricted diffusion (r = 0.271), hemorrhage (r = 0.267), blood pressure (systolic, r = 0.13; diastolic, r = 0.02). Potentially new PRES causes included contrast-related anaphylaxis and alcohol withdrawal. CONCLUSION: This large series of PRES cases shows that atypical distributions and imaging manifestations of PRES have a higher incidence than commonly perceived, and atypical manifestations do not correlate well with the edema severity.