Revista De Neurologia 

About: Revista De Neurologia is an academic journal published by Viguera Publishers. The journal publishes majorly in the area(s): Medicine & Epilepsy. It has an ISSN identifier of 0210-0010. Over the lifetime, 7632 publications have been published receiving 52672 citations. The journal is also known as: Revista de neurología (Internet).

Learning and memory

Abstract: INTRODUCTION The paper briefly reviews current knowledge on learning and memory processes, considered at the behavioral, cognitive and neural levels. DEVELOPMENT After establishing the distinction between different learning processes (behavioral learning, skill acquisition and information acquisition processes), the specific learning phenomena belonging to each of these varieties are analyzed. Associative learning is described as a behavioral (pavlovian conditioning and instrumental learning) and cognitive (predictive learning and categorization) process. Also described are the properties of perceptual and motor learning, as those of the processes by which cognitive skills (e.g., rule learning) are acquired. Then, the distinction between short-term and long-term memory is discussed, referring to short-term memory as a working memory system that assists the performance of a variety of thinking and reasoning tasks. Finally, the two main long-term memory theories are discussed, considering the semantic/episodic and implicit/explicit memory dichotomies.

Functional anatomy of the basal ganglia

Abstract: Introduction The cerebral cortex of mammals is massively interconnected with the basal ganglia. The manner in which the basal ganglia process information has been accepted since it was described in the 1980s. It is not a definitive model and many aspects of it still need clarification. Development The corpus striatum (ST) forms the entrance to the basal ganglia circuit (BG) and receives numerous afferent fibres from the cerebral cortex. Similarly, the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNpr) form the main nuclei for exit from the circuit and have an inhibitory effect on the pre-motor neurones of the ventral lamina of the thalamus. Between the entrance nucleus and the exit structures are two parallel systems of projection known as the direct and indirect pathways. The direct pathway projects monosynaptically only on the Gpi/SNpr complex. The indirect pathway projects polysynaptically on to the GR/SNpr complex after passing through the external segment of the globus pallidus (Gpe) and subthalamic nucleus. Imbalance in the activity of these two circuits will lead to alterations in discharge from the Gpi/SNpr complex which will cause bradykinesia or hyperkinesia. The bradykinesia or akinesia would be caused by increased gabaergic inhibition of the thalamic premotor neurones as a result of excessive discharge of the Gpi/SNpr complex. Conclusion Current exploration of the electrophysiology of the basal ganglia and careful analysis of the clinical findings in lesions circumscribed to certain parts of the thalamus, subthalamus and internal globus pallidus in patients with Parkinson's disease, have led to the appearance of paradoxical effects, according to the current basal ganglia model.

Diseases of mitochondrial DNA

Abstract: Introduction Human diseases caused by disorders of the mitochondrial metabolism have been described more than 30 years ago. Some of these are associated to defects in the oxidative phosphorylation system (OXPHOS system), the final pathway of the mitochondrial energetic metabolism, that leads to the synthesis of ATP. Development Part of the polypeptide subunits involved in the OXPHOS system are codified by the mitochondrial DNA (mtDNA). In the last 12 years, mutations (point mutations or deletions) in the mtDNA have been described and associated to well defined clinical syndromes caused by defects in the OXPHOS system. The clinical features of these diseases are very heterogeneous affecting in most cases to a great variety of organs and tissues. Conclusions The correct diagnosis of these mitochondrial disorders require precise clinical, morphological, biochemical, and genetic data. The rapid advances in genetic analysis allow the rapid detection of mutations, even before the obtention of other type of analysis.

Neurological complications of coronavirus and COVID-19.

Abstract: Introduction Clinical and experimental studies have shown that the coronavirus family has a certain tropism for the central nervous system. Seven types of coronavirus can infect humans. Development Coronaviruses are not always confined to the respiratory tract, and under certain conditions they can invade the central nervous system and cause neurological pathologies. The potential for neuroinvasion is well documented in most human coronaviruses (OC-43, 229E, MERS and SARS) and in some animal coronaviruses (porcine haemagglutinating encephalomyelitis coronavirus). Neurological symptoms have been reported in patients affected by COVID-19, such as headache, dizziness, myalgia and anosmia, as well as cases of encephalopathy, encephalitis, necrotising haemorrhagic encephalopathy, stroke, epileptic seizures, rhabdomyolysis and Guillain-Barre syndrome, associated with SARS-CoV-2 infection. Conclusions Future epidemiological studies and case records should elucidate the real incidence of these neurological complications, their pathogenic mechanisms and their therapeutic options.

[Monogenic causes of X-linked mental retardation].

Abstract: INTRODUCTION AND DEVELOPMENT The term X-linked mental retardation (XLMR) refers to a heterogeneous group of conditions that, on the basis of their presenting symptoms, have traditionally been classified as being syndromic (SMR) and non-syndromic or non-specific (XMR). The prevalence of XLMR in males is estimated to be 10%, excluding fragile X syndrome, which is the most common monogenic cause. There are over 100 genes involved in XLMR. In this work we review some of the phenotypes and genes involved in SMR. A small stature and coarse features indicate a suspected case of Coffin-Lowry syndrome, which is secondary to mutations of the RPS6KA3 or RSK2 genes. Cerebellar hypoplasia points towards alterations of the OPHN1 gene. In males with coarse features and genital abnormalities screening for alpha thalassemia must be carried out; this association results from mutations in the ATRX gene. Of the genes involved in mental retardation and epilepsy, the most notable are SLC6A8 (which triggers a deficit in creatine transport when altered and which is easily detected with respect to its biochemistry) and ARX (also associated to lissencephaly and dystonia of the hands). Mutations in the PQBP1 and JARID1C genes have been identified in patients with mental retardation associated to microcephaly and short stature. A high level of T3 hormone points towards defects in the SLC16A2 gene. Some of these genes have also been implicated in XMR, which makes this distinction less clear molecularly speaking. CONCLUSIONS Systematic screening of all the genes involved in XLMR is not possible in clinical praxis today. It is important to search for differential phenotypic features in males with mental retardation that guide the study towards specific genes. Identification of the molecular defect will allow for correct genetic counselling. DNA microarrays for the study of different mutations in a large number of genes involved in mental retardation are the great hope for the future.