No abstract

The carotid ring sign helps to differentiate acute from chronic carotid occlusion. If further confirmed, this information may be helpful in studying ischemic symptoms and selecting treatment strategies in patients with carotid occlusions.

SUMMARYIn February 2011, the Food and Drug Administration informed that prescription of proton pump inhibitor (PPI) drugs may cause low serum magnesium levels if taken for prolonged periods of time. We present an ex-smoker, 76-year-old man, with high blood pressure, diabetes mellitus and Barrett's oesophagus (treated with esomeprazole since 2003) admitted due to fluctuating aphasia. Neurovascular and neuroimaging studies were normal. Dyslipidemia and atrial arrhythmia were discovered. The patient was discharged with the diagnosis of left middle cerebral artery transient ischaemic attack and anticoagulation treatment was recommended. The patient returned to the emergency department on further two occasions (confusional episodes) and was admitted in order to complete the neurological study that was normal. The patient was discharged with the diagnosis of probable epileptic seizures. After a week, he was admitted due to generalised temblor and unsteadiness. A complete blood test was performed and showed a severe hypomagnesaemia (not previously performed). BACKGROUND

Cerebral vasoconstriction is a normal physiological response under determined conditions to preserve a normal cerebral blood flow. However, there are several syndromes, with impaired cerebral autoregulation and cerebral vasoconstriction, not related with infection or inflammation, which share the same radiological and clinical presentation. We review here the cerebral hyperperfusion syndrome and related conditions such as hypertensive encephalopathy, posterior reversible encephalopathy syndrome, and reversible cerebral vasoconstriction syndrome. These syndromes might share the same pathophysiological mechanism with endothelial damage, cerebral vasoconstriction, blood-brain barrier disturbance, cerebral edema, and, occasionally, intracerebral hemorrhage, with fatal cases described in all. Despite knowledge of these syndromes, they still remain unknown to us. Why these entities present in some patients and not in others goes further than the actual understanding of these diseases. We have to consider that a genetic susceptibility and molecular disturbances may be involved. Thus, more studies are needed in order to better characterize such syndromes.

Early clinical profiles of evolution in thrombolysed patients vary considerably. Even with CI, it is critical to maintain vessel permeability to avoid subsequent CW.