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Introduction: Transient ischaemic attack (TIA) has classically been defined as an episode of self-limited focal neurological deficit lasting up to 24 hours, with no neuroimaging evidence of established acute ischaemic injury. However, the definition of this entity is changing, and is adapting to new times and new diagnostic techniques, including magnetic resonance imaging (MRI) with diffusion sequences. An early and comprehensive approach to TIA, including MRI, is important to rule out clinically recovered established ischaemic strokes, in order to optimise the diagnostic and therapeutic management of patients., Patients and Methods: Patients admitted to our stroke unit over a six-month period with suspected TIA were identified, and the definitive diagnosis and approach was studied based on the tests performed., Results: A sample of 106 suspected cases of TIA were studied, in which early MRI was performed. Of these, 42 (39.62%) were clinically recovered ischaemic strokes (CRIS); 32 (30.18%), other pathologies (six epileptic seizures, five migraine auras, nine functional disorders, two amyloid spells and nine other causes, totalling 31); 26 (24.52%), TIAs; and six (5.66%), haemorrhagic stroke. Of 43 CRIS, eight (18.6%) were cardioembolic; eight (18.6%), atherothrombotic; eight (18.6%), embolic stroke of unknown origin; six (13.95%), lacunar stroke; five (11.62%) of infrequent cause; and four (9.3%), totalling 39, of undetermined cause. CRIS patients received significantly more individualised therapeutic management than TIA patients., Conclusions: The early use of MRI in the clinical suspicion of TIA makes it possible to gather evidence of CRIS and optimises the diagnostic and therapeutic approach for patients.

Introduction: Memory loss is an increasingly frequent reason for consultation in neurology. The aim of this work is to know the current frequency as well as the characteristics and disorders of the patients who come for this reason., Methods: We studied 200 patients who came to general neurology consultation due to loss of memory., Results: 18.47% of the patients who came for the first time to a general neurology consultation did so due to memory loss, this being subjective loss of memory (SLM) in 39% of the cases and referred loss of memory (RLM) in 61% of the cases. The diagnostic groups to which the patients belonged are, in diminishing order, the following: degenerative primary dementia type Alzheimer's disease, mild cognitive impairment, mixed dementia, pure vascular dementia, depressive pseudodementia, attributable to drugs, secondary to systemic disease, non-Alzheimer's type disease primary degenerative dementia, structural reasons, transitory global amnesia and epilepsy. No disease was found in 13% of them, and the generally came due to SLM., Conclusions: Frequency of memory loss as a reason for consultation continues to growing. Patients studied due to memory loss, in whom no disease is found, are generally those having SLM. In spite of this, SLM is a good predictor of cognitive deterioration. It is important to systematically study of every patient and consults for loss of memory and to investigate the possible use of drugs or toxics that could alter the memory.

Introduction: Prion encephalopathies are a group of diseases with a hereditary or acquired origin which, after a long asymptomatic period, give rise to rapidly progressing neurological disorders. This progression can only be explained by an exponential growth of the pathogenic protein load, which allows to keep the load in low levels for many years and then to grow swiftly in a few months., Development: Bearing in mind the knowledge currently available about the pathogenesis of prion diseases and patients' clinical progression, it becomes possible to distinguish several different periods of progression, the length of which can be estimated for each disease by reviewing the series of cases published to date. In general, the infectious prion diseases have a shorter period of latency than the hereditary ones and those caused by insertion of genetic material are associated to shorter latencies and to longer periods of illness than those caused by sporadic mutations., Conclusions: The rate of growth of the prion load depends essentially on how fast the pathogenic prion protein replicates; nevertheless, this growth is also modulated by other factors, many of which are polymorphisms in certain positions on the gene coding for prion protein or in other genes.