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The internal jugular veins are considered to be the main pathways of cerebral blood drainage. However, angiographic and anatomical studies show a wide anatomical variability and varying degrees of jugular and non-jugular venous drainage. The study systematically analyses the types and prevalence of human cerebral venous outflow patterns by ultrasound and MRI. Fifty healthy volunteers (21 females; 29 males; mean age 27+/-7 years) were studied by color-coded duplex sonography. Venous blood volume flow was measured in both internal jugular and vertebral veins in the supine position. Furthermore, the global arterial cerebral blood volume flow was calculated as the sum of volume flows in both internal carotid and vertebral arteries. Three types of venous drainage patterns were defined: a total jugular volume flow of more than 2/3 (type 1), between 1/3 and 2/3 (type 2) and less than 1/3 (type 3) of the global arterial blood flow. 2D TOF MR-venography was performed exemplarily in one subject with type-1 and in two subjects with type-3 drainage. Type-1 drainage was present in 36 subjects (72%), type 2 in 11 subjects (22%) and type 3 in 3 subjects (6%). In the majority of subjects in our study population, the internal jugular veins were indeed the main drainage vessels in the supine body position. However, a predominantly non-jugular drainage pattern was found in approximately 6% of subjects.

Nearly half a century after the first report of normal pressure hydrocephalus (NPH), the pathophysiological cause of the disease still remains unclear. Several theories about the cause and development of NPH emphasize disease-related alterations of the mechanical properties of the brain. MR elastography (MRE) uniquely allows the measurement of viscoelastic constants of the living brain without intervention. In this study, 20 patients (mean age, 69.1 years; nine men, 11 women) with idiopathic (n = 15) and secondary (n = 5) NPH were examined by cerebral multifrequency MRE and compared with 25 healthy volunteers (mean age, 62.1 years; 10 men, 15 women). Viscoelastic constants related to the stiffness (µ) and micromechanical connectivity (α) of brain tissue were derived from the dynamics of storage and loss moduli within the experimentally achieved frequency range of 25-62.5 Hz. In patients with NPH, both storage and loss moduli decreased, corresponding to a softening of brain tissue of about 20% compared with healthy volunteers (p < 0.001). This loss of rigidity was accompanied by a decreasing α parameter (9%, p < 0.001), indicating an alteration in the microstructural connectivity of brain tissue during NPH. This disease-related decrease in viscoelastic constants was even more pronounced in the periventricular region of the brain. The results demonstrate distinct tissue degradation associated with NPH. Further studies are required to investigate the source of mechanical tissue damage as a potential cause of NPH-related ventricular expansions and clinical symptoms.

Lumbar spinal stenosis (LSS) comprises narrowing of the spinal canal with subsequent neural compression, and is frequently associated with symptoms of neurogenic claudication. To establish a diagnosis of LSS, clinical history, physical examination results and radiological changes all need to be considered. Patients who exhibit mild to moderate symptoms of LSS should undergo multimodal conservative treatment, such as patient education, pain medication, delordosing physiotherapy and epidural injections. In patients with severe symptoms, surgery is indicated if conservative treatment proves ineffective after 3-6 months. Clinically relevant motor deficits or symptoms of cauda equina syndrome remain absolute indications for surgery. The first randomized, prospective studies have provided class I-II evidence that supports a more rapid and profound decline of LSS symptoms after decompressive surgery than with conservative therapy. In the absence of a valid paraclinical diagnostic marker, however, more evidence-based data are needed to identify those patients for whom the benefit of surgery would outweigh the risk of developing complications. In this Review, we briefly survey the underlying pathophysiology and clinical appearance of LSS, and explore the available diagnostic and therapeutic options, with particular emphasis on neuroradiological findings and outcome predictors.