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Introduction: Chronic migraine refractory to preventive treatment is a common clinical situation in general neurology clinics. The aim is to analyse our experience with zonisamide in the preventive treatment of patients with frequent refractory migraine., Patients and Methods: Those patients with no response or intolerance to topiramate and at least one more preventative received zonisamide. This drug was increased 25 mg per week up to 200 mg/day. The efficacy of zonisamide was evaluated in terms of 'response' (reduction in attack frequency below 50%) at the third month of treatment., Results: Our series comprises a total of 172 patients, with ages ranging from 22 to 69 years. 85% were women. The final dosage of zonisamide was 50-200 mg/day, with the 100 mg/day being the most frequently administered dose. Zonisamide was efficacious (response) in 76 (44%) patients; response being excellent in 22 (13%). MIDAS score was reduced by 43.2%. Zonisamide was not tolerated by 27% of the patients, mainly due to subjective mental slowness or digestive symptoms., Conclusions: These results, obtained in a big sample of patients refractory or intolerant to topiramate and other preventatives, indicate that, at least in conditions of daily clinical practice, zonisamide, at relatively low dosages, is an option to be considered for the preventive treatment of patients with frequent migraine.

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.

Introduction: The anatomy of the upper cervical region, in the presence of structural anomalies favours the compression of the brachial plexus and/or subclavian vessels, giving rise to the thoracic inlet syndrome (SATS). Neurological involvement is more common than vascular involvement (95 and 5% respectively); the latter is known as the arterial SATS. The forms of clinical presentation of arterial SATS are very variable and have different prognoses: it may present as acute distal ischaemia with a variable course, peripheral embolism or as a non-serious condition such as Raynaud's phenomenon., Clinical Case: We present a case with arterial involvement only, associated with a clavicular osteophyte, in a patient with episodes of acute, transient weakness of the arm which were initially thought to be transient strokes with brachial monoparesis., Conclusion: Classically, the basic examination to diagnose arterial SATS has been conventional angiography, an invasive test which is not without complications; in our case it was magnetic angioresonance which showed changes in blood flow on forced arm movement. This avoided having to do a conventional angiogram. Angioresonance, rarely cited in this syndrome, is worthy of study and comparison with the 'standard' diagnostic method of conventional angiography.