[Hemifacial spasm as manifestation of benign intracranial hypertension. Letter].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
P Serrano-Castro
Publications and source records attributed to P Serrano-Castro.
[Mesial temporal sclerosis (I): histological data, physiopathological hypothesis and etiological factors].
OBJECTIVE: To review the main anatomical, histological, physiopathological and aetiological data characteristic of the mesial temporal sclerosis syndrome (ETM). Development. The typical histological findings in ETM are: 1) A specific pattern of loss of neurone density which includes so-called endfolium sclerosis (considered to be a specific pathological entity always found in ETM), and which is usually accompanied by neurone loss in other hippocampal and extra-hippocampal regions. The CA2 region is never affected. 2) Phenomenon of 'mossy fibers sprouting' which are granulosa cells which form two types of synapses: with the the 'basket cells' which are inhibitory interneurones and with the dendrites of granulosa or pyramidal cells of the CA1, CA2 and CA3 Ammon horn cells which are excitatory cells. CONCLUSIONS: Probably these organic changes are both the cause and effect of repeated convulsions. Participation in this self-perpetuating circuit may be due to recognised risk factors of ETM (head injury, CNS infections, febrile convulsions in early stages of development) which cause, first of all, death of neurones of the dentate gyrus cells followed by reduced inhibitory activity of the 'basket' cells and therefore sustained hyper-excitability of the pyramidal cells (especially in the CA3 regions), which are responsible for complex partial seizures and massive liberation of glutamic acid. Glutamic acid can cause death of neurones of the granulosa cells of the dentate gyrus, thus closing the circuit. This hypothesis explains the progressive nature of the ETM syndrome. When there is pathology of the cortical structure there is another access via to this circuit--by means of cortical discharges of the so-called perforant pathway which stimulates activity of the pyramidal cells and sets off the chain of events described above. This hypothesis explains the so-called 'dual pathology'.
Brain Injuries↗
[Refractory epilepsy in adults].
AIMS: Between 25 33% of epileptic patients continue to present epileptic seizures in spite of adequate treatment with antiepileptic drugs (AED). This fact has led to a gradual development of new AED, a progressive expansion of epilepsy surgery and a great amount of interest in the overall knowledge of patients with refractory or AED resistant epilepsy. METHOD: Refractory epilepsy (RE) can be defined as the persistence of correctly diagnosed epileptic seizures that recur so often that they interfere in patients daily lives, after having received treatment with two best choice AED and an association at maximum tolerable doses for two years, which can be less in very acute crises. There exist factors that allow us to forecast a bad prognosis and diagnostic or therapeutic mistakes that point to a pseudorefractory condition must always be excluded. In treating this disorder, we must confirm that there are seizures, as well as the existence or absence of lesions as a substratum, and guarantee suitable treatment with some basic guidelines. Surgery is currently an efficient, safe form of therapy in a group of patients with RE and must be proposed as early as possible when it is suitably indicated, since it eliminates a high percentage of the seizures. If surgery or other alternative treatment does not control the seizures, in the long run therapy should be optimised to try to eliminate the most aggressive seizures and the chronic intoxication by AED in order to provide a better quality of life. CONCLUSION: New therapeutic resources are needed to prevent the negative irreversible consequences of uncontrolled epileptic seizures
Adult↗