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Background and Purpose: The purpose of this article is to assess the validity of the magnetic resonance imaging (MRI) CISS 3D sequence associated with 3D time of flight (TOF) angiographic sequence in order to detect neurovascular contact (NVC) between the facial nerve and neighbouring arteries in patients with essential hemifacial spasm (HFS) and to determine the relationship between HFS symptoms and NVC and NVC image features (type, number and site)., Materials and Methods: We prospectively enrolled 120 cerebellopontine angle (CPA) MRI studies, 44 cases with HFS symptoms and 76 which were asymptomatic (controls), using axial T2-weighted (CISS) and axial 3D TOF series with associated Maximal intensity (MIP) reconstructions. Prior TOF angiographic studies were available for 56 cases without associated CISS images and the results obtained from that study were compared with the results of the current study., Results: The diagnostic values obtained significantly favoured the protocol used in this study, which demonstrated a sensitivity of 77.27% and a specificity of 75%. There was a statistically significant relationship between the presence of NVC and HFS symptoms (p<0.0001). Only one statistically significant relationship was found between facial nerve displacement (in type of NVC) and HFS symptoms (p=0.019)., Conclusions: The proposed MRI protocol is sensitive and valid for detecting NVC in patients with HFS. The results of our study support a relationship between NVC and HFS symptoms. It is not a simple relationship, however. It may be influenced by other factors, such as displacement of the facial nerve due to NVC.

Objective: The atherosclerosis is the most common cause of death and disability in developed countries by causing ischemic cardiopathic and stroke. The ischemic atherotrombotic stroke is the most frequent form of the last one. In this sense we review herein the mechanisms underlying the artherosclerotic process., Development: It is understood as an inflammatory disease, by taking into account the widely accepted hypothesis by Ross: it was firstly stated in structural terms, as macrophages and T/B linfocities were present in the arterial wall from the first stages of the disease (fatty streak) to the last and complicated ones. The starting point is a functional endothelial damage, secondary to mechanical or vascular risk factors and called response to injury hypothesis . The next step is an inflammatory cascade that involves humoral (citokines, growth factors) and cellular (increased quimiotaxis, adherece and infiltration of inflamatory cells) mechanisms. They interact among them, outbalanced and in a progresssive way that leads to the final fibroproliferative response. Every stage has his own inflammatory components and interactive pathways. The following elements are outstanding in this process: 1) Adhesion molecules, including E selectin, ICAM 1 and VCAM 1, that are increased locally in the plaques and as circulating elements; plaquetary receptors of the type IIb/IIIa are integrins wich belong to the same family; 2) Citokines with either proinflammatory activity like IL 1, the TNF a and linfocitary ligands like the CD 40, or with antiinflammatory activity like the gamma interpheron; 3) Growth factors, with plaquetary (PDGF) and fibroblastic (FGF) variants as the cornerstone; 4) Markers of systemic inflammation, overall plasma C reactive protein and fibrinogen, that predict the risk of stroke and cardiovascular death; IL 6, complement, thrombin and heat shock proteins (HSP) would act in a similar but less conclusive way., Conclusions: The evidences of the pivotal role of the inflammation in the stroke allow to develop therapeutical strategies to prevent the disease: fostering natural antiinflamatory mechanisms, or inhibiting inflammatory elements by selective (monoclonal antibodies) or non selective (IIb/IIIa receptors, antiinflammatory drugs) pathways are distinctily glimpsed, ongoing or fully developed.