BACKGROUND AND PURPOSE: Patients with idiopathic intracranial hypertension have transverse sinus stenosis on gadolinium-bolused MRV, but other MR imaging signs are less consistently seen. Our aim was to demonstrate that transverse sinus stenosis could be identified on conventional MR imaging, and this identification would allow improved diagnostic sensitivity to this condition. MATERIALS AND METHODS: MR imaging and MRV images from 63 patients with idiopathic intracranial hypertension and 96 controls were reviewed by using 3 independent procedures. MRV images were graded for the presence and degree of stenosis of the transverse sinus. Postgadolinium coronal T1-weighted sequences were evaluated independent of MRV. The dimensions of the proximal and distal transverse sinus were measured from the MRV examinations, and the cross-sectional area of the transverse sinus was calculated. Correlation among the 3 modes of evaluation of the transverse sinus was conducted by using Wilcoxon/Kruskal-Wallis, Pearson, and Spearman ρ nonparametric statistical techniques. RESULTS: Transverse sinus stenosis was identified bilaterally on MRV in 94% of patients with idiopathic intracranial hypertension and in 3% of controls. On coronal T1 postgadolinium MR images, transverse sinus stenosis was identified in 83% of patients with idiopathic intracranial hypertension and 7% of controls. Previously described MR imaging signs of intracranial hypertension were identified in 8%–61% of patients with idiopathic intracranial hypertension. Correlation among the 3 modes of evaluation was highly significant (P < .0001). CONCLUSIONS: Even without the assistance of an MRV sequence, neuroradiologists can validly identify bilateral transverse sinus stenosis in patients with intracranial hypertension more reliably than other previously described MR imaging findings in this condition. We conclude that transverse sinus stenosis is the most useful and sensitive imaging indicator of this disease state.

An incidental finding (IF) in human subjects research is defined in a major consensus project as an observation “concerning an individual research participant that has potential clinical importance and is discovered in the course of conducting research, but is beyond the aims of the study.”^1(p219) Numerous reports have detailed how the detection of an IF can result in the early beneficial diagnosis of an unsuspected malignant neoplasm or aneurysm.^2-5 However, others describe harm and excessive cost resulting from treatment of radiographically suspicious IFs.^6,7 Moreover, clinical experience dictates that many IFs are of indeterminate clinical significance and generate uncertainty among both research participants and their physicians.⁶

Acquired copper deficiency presents with a spastic gait and sensory ataxia. Spinal cord magnetic resonance imaging (MRI) in patients with copper deficiency myelopathy may show increased T2 signal, most commonly in the dorsal midline cervical and thoracic cord. These imaging findings may be reversible with normalization of serum copper. The clinical and imaging picture is very similar to the subacute combined degeneration seen in patients with vitamin B12 deficiency. Neuroradiologists should consider this possibility when a long segment of symmetric dorsal spinal cord T2-hyperintensity is identified.

Several cerebral pathologic processes thought to result from derangements in vascular autoregulatory mechanisms show reversible abnormalities on computed tomographic and magnetic resonance images. The hypertensive encephalopathies are characterized by intracranial abnormalities due to subacutely elevated blood pressure; these entities include hypertensive encephalopathy, preeclampsia and eclampsia, and cyclosporine toxicity. Imaging studies reveal symmetric confluent lesions with mild mass effect and patchy enhancement centered in the immediate subcortical white matter of the occipital lobes. The uremic encephalopathies are characterized by intracranial abnormalities due to an elevated level of blood urea nitrogen; these entities include uremia and glomerulonephritis, hemolytic-uremic syndrome, and thrombotic thrombocytopenic purpura. Imaging studies reveal multiple areas of symmetric edema in the basal ganglia; in severe cases, focal infarcts with or without hemorrhage can be seen. As radiologists become more familiar with these entities, cases can be recognized earlier in the disease process, allowing more timely initiation of appropriate therapy.

Food intake regulation in humans is a complex process controlled by the dynamic interaction of homeostatic and hedonic systems. Homeostatic regulation is controlled by appetitive signals from the gut, adipose tissue, and the vagus nerve, while conscious and unconscious reward processes orchestrate hedonic regulation. On the one hand, sight, smell, taste, and texture perception deliver potent food-related feedback to the central nervous system (CNS) and influence brain areas related to food reward. On the other hand, macronutrient composition stimulates the release of appetite signals from the gut, which are translated in the CNS into unconscious reward processes. This multi-level regulation process of food intake shapes and regulates human ingestive behavior. Identifying the interface between hormones, neurotransmitters, and brain areas is critical to advance our understanding of conditions like obesity and develop better therapeutical interventions. Neuroimaging studies allow us to take a glance into the central nervous system (CNS) while these processes take place. This review focuses on the available neuroimaging evidence to describe this interaction between the homeostatic and hedonic components in human food intake regulation.