Degenerative changes in the posterior paraspinal structures were found in a higher percentage of subjects with lower back pain than in controls. Use of a STIR sequence with homogeneous fat suppression facilitates visualization of these changes.

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ABSTRACT. Sciatica is the most frequently encountered symptom in neurosurgical practice and is observed in 40% of adults at some point in their lives. It is described as pain of the hip and the lower extremity secondary to pathologies affecting the sciatic nerve within its intraspinal or extraspinal course. The most frequent cause is a herniating lumbar disc pressing on the neural roots. Extraspinal causes of sciatic pain are usually overlooked because they are extremely rare and due to intraspinal causes (lumbar spinal stenosis, facet joint osteoarthritis, fracture, and tumors of the spinal cord and spinal column) being the main consideration. Early diagnosis of sciatica significantly improves the likelihood of relieving symptoms, as well as avoiding any additional neurologic injury and unnecessary surgery. We evaluate histolopathologically confirmed extraspinal causes of sciatica cases, accompanied by their presented computed tomography and/or magnetic resonance imaging findings. AnatomyBeing familiar with the anatomy of the lumbosacral plexus and sciatic nerve is essential for the evaluation of extraspinal sciatica. The lumbar plexus is composed of the ventral rami of L1-L4 and is anatomically located behind the psoas muscle. A minor branch of L4 combines with the ventral ramus of L5 to form the lumbosacral cord or trunk. The lumbosacral trunk descends over the sacral ala and combines with the ventral rami of S1, S2 and S3 (and a branch of S4) to form the sacral plexus [1].

The aim of this study was to retrospectively measure and compare pancreatic apparent diffusion coefficient (ADC) in patients with acute pancreatitis (AP) with aged matched controls who underwent diffusion weighted imaging (DWI). The institutional review board approved this retrospective Health Insurance Portability and Accountability Act compliant study with a waiver for informed consent. Pancreatic ADC values from 27 patients with a clinical diagnosis of AP and 38 normal age-matched controls evaluated with DWI (b = 0 and 800 mm(2)/s) were retrospectively and independently measured by two radiologists. The ADCs were compared between the groups and between each of the pancreatic segments in the normal group. Inter-observer reliability was calculated and receiver operating characteristic analysis was used to determine the sensitivity and specificity of DW imaging in the diagnosis of acute pancreatitis. P < 0.05 was considered statistically significant. The ICC for inter-observer reliability was 0.98 in the control and 0.97 in the AP group. The mean pancreatic ADC in the AP group (1.32 × 10(-3) mm(2)/s ± 0.13) was significantly lower than in the normal group (1.77 × 10(-3) mm(2)/s ± 0.32). There was no significant difference in mean ADCs between each of the pancreatic segments in the controls. A threshold ADC value of 1.62 × 10-3 mm(2)/s yielded a sensitivity of 93% and specificity of 87% for detecting acute pancreatitis for b values of 0 and 800 s/mm(2). Pancreatic ADCs are significantly lower in patients with AP than normal controls.

BackgroundMigraine is a common headache disorder that may be associated with vascular disease and cerebral white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI) scan. High sensitivity C-reactive protein (hs-CRP) is a marker of inflammation that may predict subclinical atherosclerosis. However, the relation between migraine, vascular risks, and WMHs is unknown. We evaluated hs-CRP levels and the relation between hs-CRP level and WMHs in adult migraine patients.MethodsThis case–control study included 432 subjects (216 migraine patients [without aura, 143 patients; with aura, 73 patients]; 216 healthy control subjects without migraine; age range 18–50 y). Migraine diagnosis was determined according to the International Classification of Headache Disorders II diagnostic criteria. The migraine patients and control subjects had no known vascular risk factors, inflammatory disease, or comorbid disease. The presence and number of WMHs on MRI scans were determined, and serum hs-CRP levels were measured by latex-enhanced immunoturbidimetry.ResultsMean hs-CRP level was significantly greater in migraine patients (1.94 ± 2.03 mg/L) than control subjects (0.82 ± 0.58 mg/L; P ≤ .0001). The mean number of WMHs per subject and the presence of WMHs was significantly greater in migraine patients (69 patients [31.9%]; 1.68 ± 3.12 mg/dL) than control subjects (21 subjects [9.7%]; 0.3 ± 1.3; P ≤ .001). However, there was no correlation between hs-CRP level and WMHs in migraine patients (r = 0.024; not significant). The presence of WMHs was increased 4.35-fold in migraine patients (odds ratio 4.35, P ≤ .001).ConclusionsHigh hs-CRP level may be a marker of the proinflammatory state in migraine patients. However, the absence of correlation between hs-CRP level and WMHs suggests that hs-CRP is not causally involved in the pathogenesis of WMHs in migraine patients. The WMHs were located mostly in the frontal lobe and subcortical area.