Enhancing and expansile portal vein thrombosis: value in the diagnosis of hepatocellular carcinoma in patients with multiple hepatic lesions.

OBJECTIVE: The objective of this study was to determine whether the presence of enhancing and expansile portal vein thrombus is suggestive of the diagnosis of hepatocellular carcinoma. CONCLUSION: In the presence of hepatic tumors, enhancing expansile portal vein thrombus is highly suggestive of hepatocellular carcinoma.

Are plain radiographs of the spine necessary during evaluation after blunt trauma? Accuracy of screening torso computed tomography in thoracic/lumbar spine fracture diagnosis.

BACKGROUND: Fracture of the thoracolumbar (TL) spine is reported in 8 to 15% of victims of blunt trauma. Current screening of these patients is done with conventional radiography. This may require repeated sets of films and take hours to days. It is imperative that these patients get timely, accurate evaluation to allow for treatment planning and early mobilization; alternatives to plain films would aid in this. The objective of this study is to determine whether the data obtained from admission chest/abdomen/pelvis (CAP) computed tomography (CT) scans after blunt trauma has utility in thoracolumbar spine evaluation. METHODS: The records of all patients admitted to a Level I trauma center over a 2-month period who underwent CAP CT were reviewed for the presence of TL spine fracture, time to completion of plain film evaluation, and clinical course. Admission CT scans were reviewed by an attending radiologist who was blinded to any previously diagnosed spine fractures. The two tests were compared for diagnostic accuracy and their discriminatory ability was compared using receiver operating characteristic (ROC) curves. Significance was defined as p < 0.05. RESULTS: In all, 103 patients were admitted from January 1, 2003 to February 28, 2003 and underwent CAP CT scan as part of their initial trauma evaluation. Of these, 26 (25%) had thoracolumbar fractures. Seven (27%) thoracolumbar fractures were not seen on plain radiographs taken during the trauma evaluation. Average time until plain film completion in this group was 8 hours (range, 44 minutes to 38 hours). All 26 (100%) patients with fractures, however, were diagnosed on CT scan performed shortly after admission. Of the remaining 77 patients, two (2.6%) were falsely read as positive for fracture on CT. Sensitivity and specificity of CT scan for thoracolumbar fracture were excellent at 100% and 97%, respectively, with a negative predictive value of 100%. Plain radiographs were 73% sensitive, 100% specific, and had a negative predictive value of 92%. Area under the ROC curve for CT was 0.98, but for plain film was 0.86 (p < 0.02). CONCLUSION: Admission CAP CT obtained as part of the routine trauma evaluation in these high-risk patients is more sensitive than plain radiographs for evaluation of the TL spine after blunt trauma. In addition, CAP CT can be performed faster. Omission of plain radiographs will expedite accurate evaluation allowing earlier treatment and mobilization.

NMDA currents and receptor protein are downregulated in the amygdala during maintenance of fear memory.

The amygdala plays a critical role in fear conditioning, a model of emotional learning and cue-induced anxiety. In the lateral amygdala, fear conditioning is associated with an enduring increase in synaptic strength mediated through AMPA receptors and with a reduction in paired-pulse facilitation, reflecting an increased probability of neurotransmitter release. Here we show that NMDA-mediated transmission in the thalamic-to-lateral amygdala pathway is not facilitated after fear conditioning, although probability of transmitter release is enhanced. Rather, the EC50 for NMDA receptor (NR)-mediated current is shifted threefold to fourfold to the right in fear-conditioned animals, suggesting a postsynaptic alteration in NMDA receptors in the maintenance phase of fear memory. Furthermore, the ability of nonselective and subunit-selective antagonists of NMDA receptors to block NMDA receptor-mediated EPSCs is reduced in lateral amygdala neurons from fear-conditioned animals, suggesting a reduction in NMDA receptors at thalamolateral amygdala synapses. In addition, Western blots show a reduction in phosphorylated-NR1, NR2A, and NR2B subunit protein expression in amygdalas from fear-conditioned animals. These data indicate that postsynaptic mechanisms are involved in synaptic plasticity in the thalamoamygdala pathway in fear conditioning and raise the possibility that: (1) downregulation of the NMDA receptor may protect against excitotoxicity of unchecked NMDA receptor recruitment during induction and consolidation of fear memories, (2) reduced NMDA current and protein may allow persistence of the "capacity to reactivate" amygdala pathways in NMDA receptor-dependent fear memories, or (3) a persistent long-term depression of NMDA transmission may occur after fear learning.

L-type voltage-gated calcium channels are involved in the in vivo and in vitro expression of fear conditioning.

Fear conditioning, a behavioral model of fear learning and cue-related anxiety, causes enhanced neuronal transmission in the thalamic to lateral amygdala pathway.(1,2) In the expression phase of learned fear, this increased transmission recorded in vitro is revealed in increased amplitudes of excitatory postsynaptic currents (EPSCs) and occlusion of paired-pulse facilitation (PPF) implicating a presynaptic increase in transmitter release. Here we examined the contribution of L-type calcium channels in fear conditioning. We measured the effect of nimodipine (Nim, 1.5-20 mg/kg), an L-type calcium channel antagonist, on fear-potentiated startle in which startle was assessed in animals receiving paired or unpaired tone and foot shock. Nim administered intraperitoneally blocked fear-potentiated startle but not baseline startle in a dose-dependent manner. We also analyzed the effect of Nim (10 micro M) in vitro on synaptic facilitation of EPSCs and PPF in slices from naïve control, unpaired control, and fear-conditioned animals. In neurons from naïve control animals, Nim had no effect on EPSC amplitude or PPF, but in slices from fear-conditioned rats, Nim reduced EPSC amplitude, suggesting the recruitment of L-type calcium channels within the fear-conditioning pathway. Nim increased PPF in slices from fear-conditioned animals, suggesting that L-type calcium channels may contribute to increased probability of release in fear conditioning. In slices from unpaired animals, Nim decreased synaptic transmission but had little effect on PPF, suggesting that stress or contextual fear learning may induce L-type channel activity in fear-conditioned and unpaired control animal groups. We also analyzed protein expression of the alpha(1C) and alpha(1D) L-type calcium channel subunits isolated from the amygdala and found that alpha(1C) protein was significantly increased in fear-conditioned animals. These findings suggest that L-type calcium channels play a role in the amygdala in cued fear conditioning and have important implications in the treatment of anxiety and in emotional learning and plasticity.