A 48-year-old woman presented to our imaging department with lumbar sciatica. The patient had a medical history of low back pain and spina bifida. A transverse section lumbar spine CT-scan, obtained with soft-tissue window setting (Fig. A, arrow) showed, a fat-density (45-HU), oblong, posterior intradural supracentimetric lesion, at level of L5-S1. The use of bone window setting revealed a spina bifida at L4-L5-S1 (Fig. B, arrow). Lumbar spine MRI performed shortly afterwards confirmed the presence of a posterior intradural supra centimetric lesion, at level of L5-S1, hyperintense on T1 (Fig. C, arrow) and T2, and hypointetense on T2 Stir weighted imaging (Fig. D, arrow), and showed that the filum terminale was attached to the aforementioned lesion.It also demonstrated that the conus medullaris was in an abdormally low position, set at the spinal level of L3-L4.Intradural spinal lipoma with tethered spinal cord was diagnosed. The patient will benefit from physiotherapy and a surgical option could be envisaged according to the clinical evolution. CommentMedullary lipomas are rare tumors that account for approximately 1% of all spinal cord tumors. In children, they are responsible for tethered spinal cord syndrome in 25% to 30% of cases. The main anatomical features of this syndrome include a stretched and thickened filum terminale (over 2 mm), a conus medullaris located below L2, and a spinal cord that is attached to the posterior wall of the dural sac (by the lipoma). The most common causes of tethered spinal cord syndrome are spinal lipomas (including intradural lipomas, lipomyelomeningocele and lipoma of the filum terminale), which account for 72% of all cases. Other causes include thin filum terminale (< 2 mm in diameter) of no fatty consistency, diastematomyelia and myelomeningocele.Three clinical syndromes can be distinguished: the neuro-orthopedic syndrome, which associates sensory, motor, and trophic deficits (pain being the main symptom in adults), the lumbosacral cutaneous syndrome, which associates a dermal sinus, a subcutaneous swelling, or an angioma (absent in 70% of cases in adults, but at least one lesion is present in 90% of cases in children), and sphincter disorders (80% of all cases).As in all other spinal cord lesion, MRI provides the best imaging technique for spinal dysraphism. It is an essential technique for the preoperative assessment of this type of lesion, as CT-scans offer poor soft tissue discrimination, and don't allow sufficient study of the spinal cord, or its relation to the lipoma.Lipomas spontaneously appear hyperintense on T1, and isointense relative to subcutaneous fat on T1 and T2. The use of gadolinium is of no interest as there would be no signal modification.

Background:A 19-year-old man was referred to the orthopedist with a history of progressive pain, swelling and limitation of movement of his right elbow. Conventional radiographs had been taken one and a half year ago, at the occasion of trauma, and were repeated at the current consultation. Furthermore, patient underwent CT-Arthrography of the elbow, followed by ultrasonography after the intra-articular injection and finally MRI of the right elbow.

We report the case of a neonate born at 38 4/7 weeks of gestation with median birth weight and size and in the 75 th percentile for head circumference. Routine pregnancy follow up allowed the antenatal discovery of azygos continuation with absence of the inferior vena cava.Within the framework of a polymalformative assessment a low dose thoraco-abdominal angioscanner showed a complete absence of the suprarenal and retrohepatic segments of the inferior vena cava (Fig. D, white arrow) while a substitute collateral circulation was provided by a dilated right intercostal vein (Fig. C), white arrow which appeared to be in continuity with the supradiaphragmatic azygos vein. The arch of the azygos vein was also dilated (Fig. A, B, white arrow). CommentAbsence of the retrohepatic segment of the inferior vena cava with azygos continuation is a rare congenital anomaly with a current prevalence of 0,6% (1).In order of frequency, it represents the second most common systemic venous return anomaly, after persistent left superior vena cava (1).Once frequently associated with severe congenital heart diseases, as well as polysplenia and asplenia, it is nowadays, since the advent of cross-sectional imaging, incidentally diagnosed in asymptomatic patients (1).Azygos continuation and absence of the inferior vena cava can be diagnosed using classic imaging techniques such as radiography, ultrasound, CTscanner and MRI.The aforementioned techniques will reveal absence of the retro-hepatic segment of the inferior vena cava and drainage of the hepatic veins into a short inferior vena cava segment, or directly into the right atrium.They will also demonstrate a blind-ended inferior vena cava at its cranial margin at level of renal pedicle, as well as an azygos vein of practically equal calibre to that of the aorta, in the classic forms.In our case, only the supradiaphragmatic segment of the azygos vein and its arch appear dilated, and communicate with a dilated right intercostal vein, which in turn communicates with the right renal vein.Also, we notice a hypoplastic infradiaphragmatic azygos vein associated with an increased (left) hemiazygos vein calibre.Congenital vascular anatomical variations, and in particular, inferior vena cava and azygos venous system congenital variations with azygos continuation are important to recognize and describe in order to avoid any diagnostic errors in the supradiaphragmatic and mediastinum region.Preoperative assessment of the cardiovascular surgical patient requires an adequate knowledge of vascular anatomical variations and malformations.The prognosis of azygos continuation depends on associated cardiac anomalies.

A 34-year-old white woman presented for holocephalic headaches following a blow to the head. She did not mention any vision disturbance. Computed tomography was performed and displayed bilateral calcific deposits in the disk optic areas consistent with optic nerve head drusen. CommentOptic nerve head drusen (ONHD) is an uncommon condition, resulting from intra-and extracellular mucoproteinic deposits in the optic nerve. These deposits, called "drusen bodies" , gradually enlarge and tend to calcify. Other threatening ocular conditions seem to be associated including vascular occlusions, choroidal neovascular membrane (CNVM) and retinal hemorrhages.The prevalence of the disease in the adult population is about 0.34% and can reach 3.4% in individuals with a family history of ONHD suggesting an autosomal dominant inheritance pattern with incomplete penetrance. Drusen bodies are usually bilateral (70-80%) and more commonly affect Caucasians. There is no gender predilection.Slowly progressive peripheral visual field loss is the main symptom and occurs in 75% of patients. In contrast, central visual loss seems to be rarer and needs to rule out other causes such as tumor.Diagnosis of superficial drusen is generally made with dilated fundoscopic examination. ONHD typically shows yellow bumpy deposits over the optic disc and often gives the appearance of an edematous optic nerve with abnormal vascular patterns. B-scan ultrasonography and computed tomography (CT) are useful modalities to detect deeply buried drusen. The main differential diagnostics are true papilledema, anterior ischemic optic neuropathy, calcified granuloma, astrocytoma and optic nerve glioma.On CT imaging, drusen appear as rounded calcifications in the superficial layers of the optic disc (Fig. A, B). CT presents several disadvantages: exposure to ionizing radiation, high cost and the risk of false negatives. This is due to the tiny diameter of drusen ranging from 0.05 mm to 0.75 mm. Thus, thin-slice CT images are required. B-scan is clearly superior to highlight ONHD but CT remains interesting if clinical presentation leads to a suspicion of intracanial lesion.Currently, there is no treatment for progressive vision loss due to ONHD. Some clinicians prescribe ocular hypotensive agents in order to prevent further optic nerve damages. With regard to CNVM, different treatments have been reported: laser photocoagulation, photodynamic therapy and surgical removal.