The present study evaluated the venous anatomy of the craniocervical junction, focusing on the suboccipital cavernous sinus (SCS), a vertebral venous plexus surrounding the horizontal portion of the vertebral artery at the skull base. MR imaging was reviewed to clarify the venous anatomy of the SCS in 33 patients. Multiplanar reconstruction MR images were obtained using contrast-enhanced three-dimensional fast spoiled gradient-recalled acquisition in the steady state (3-D fast SPGR) with fat suppression. Connections with the SCS were evaluated for the following venous structures: anterior condylar vein (ACV); posterior condylar vein (PCV); lateral condylar vein (LCV); vertebral artery venous plexus (VAVP); and anterior internal vertebral venous plexus (AVVP). The SCS connected with the ACV superomedially, with the VAVP inferolaterally, and with the AVVP medially. The LCV connected with the external orifice of the ACV and superoanterior aspect of the SCS. The PCV connected with the posteromedial aspect of the jugular bulb and superoposterior aspect of the SCS. The findings of craniocervical junction venography performed in eight patients corresponded with those on MR imaging, other than with regard to the PCV. Contrast-enhanced 3-D fast SPGR allows visualization of the detailed anatomy of these venous structures, and this technique facilitates interventions and description of pathologies occurring in this area.

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Intraventricular insulin potentiates the anorexic effect of corticotropin releasing hormone in rats. Am J Physiol Regul Integr Comp Physiol 283: R1321-R1326, 2002 10.1152/ajpregu.00521.2001.-Intraventricular corticotropin releasing hormone (CRH) suppresses food intake and body weight as a stress response. Insulin, acting within the brain, also suppresses food intake and body weight, and this suppression is related to caloric homeostasis. We determined if increased insulin within the brain potentiates the anorexic effects of intraventricular CRH. Rats were food deprived for 17 h each day and then given 30-min access to Ensure. One-half received continuous third ventricular infusion of synthetic cerebrospinal fluid via osmotic minipumps, and one-half received insulin (0.6 mU/ day). During the infusion, rats also received 0, 0.1, 1.0, or 5.0 g of CRH into the lateral ventricle just before access to Ensure. Insulin alone had no effect on Ensure intake or body weight. CRH dose dependently reduced Ensure intake in both groups, and the reduction was greater in the insulin group. Hence, central insulin potentiated the ability of centrally administered CRH to suppress food intake. These findings suggest that stress-related influences over food intake, particularly those mediated via CRH, interact with relative adiposity as signaled to the brain by central insulin.food intake; body weight; obesity; satiety SOON AFTER ITS INITIAL DISCOVERY and characterization (58,74,75), the 41-amino acid peptide corticotropin releasing hormone (CRH) was found to suppress food intake when administered intracerebroventricularly to rats (18,39). This effect is now well established (46,48), and the observation has been extended to other species (31,49,55,60). CRH-elicited anorexia is thought to reflect an endogenous stress response (36,37,39,45,57), and stress-induced anorexia is attenuated by antagonists or antibodies to CRH (37, 70). The observation that expression of the CRH-2 receptor gene is reduced in food-deprived rats (72) suggests that food deprivation-induced stress is also mediated via CRH signaling. The anorectic site of action of CRH has been suggested to be in closely linked nuclei in the ventral hypothalamus, including the paraventricular and ventromedial hypothalamic nuclei (35, 36) and the medial preoptic area (23).When CRH is administered on a daily basis, it reduces body weight of rats. This occurs when CRH is given as a daily intraventricular bolus (38) as well as when it is infused 24 h/day (4, 5). Although the effect is apparent in normal (lean) rats (3-5), it is accentuated in several models of obesity, including rats with lesions of the ventromedial nuclei of the hypothalamus (4) and genetically obese Zucker (fatty) rats (3, 59). In fact, CRH has been reported to prevent hyperphagia and weight gain in young, rapidly growing fatty Zucker rats (59). That same group later provided evidence for an altered CRH system in the brain (16) and hypothalamo-pituitary-adrenal axis (33) in fatty Zucker rats. The important points a...