Spontaneous intracranial hypotension: quick clinical and magnetic resonance imaging response to corticosteroids. A case report.
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Biomedical subjects
Publications and source records attributed to F Morales-Asín.
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OBJECTIVE: The aim of our study was to investigate the possible effect of acenocoumarol, which is indicated for nonneurological disease, on headache. BACKGROUND: It has been suggested that anticoagulation can have beneficial effects in the control of migraine attacks. METHODS: Four hundred randomized patients on oral anticoagulant therapy were asked to complete a questionnaire regarding their headaches. RESULTS: Headache was present before or during oral anticoagulation in 166 (66 migraineurs and 100 nonmigraineurs) of 326 respondents. The major finding was that oral anticoagulation produced improvement in 63% of patients with migraine versus 38% of patients with nonmigranous headache. Improvement was related to the severity of migraine but not to age. CONCLUSIONS: Oral anticoagulant therapy can improve migraine. The way in which anticoagulant therapy acts on migraine is unknown, but potential mechanisms include its effect on platelet aggregability and pharmacological effects such as suppression of enhanced nitric oxide.
Three new cases compatible with hypnic headache syndrome (HHS) are presented. The patients were 70, 77, and 79 years of age (2F, 1M). They described a history of nocturnal headache ranging from 5 months to 7 years. One patient was afflicted with diffuse pain but the other two had unilateral pain. In one patient headache was clearly related with dreams, but in the other two this point could not be confirmed. Except for headache being unilateral in two cases, the remaining HHS criteria were present. It is noteworthy that pain responded to flunarizine in two patients.
OBJECTIVE: To study the relationship between the hormone response to stress seen after ACV (CVA) and the type, size and site of the lesion. MATERIAL AND METHODS: We made a prospective study of the relationship between stress hormones and the radiological characteristics of the lesion in 82 patients admitted to hospital for non AIT ACV (CVA). We assessed the 24 hour urine catecholamines (total catecholamines, adrenaline, noradrenaline, vanillylmandelic acid, metanephrines and dopamine) and the 24 hour urine cortisol, collected on the second and third day after admission respectively. The type, size and site of the lesions were studies on CT scans done between 3 and 7 days after admission. RESULTS: We studied 82 patients, 43 men and 39 women with an average age of 71.7. In 7 patients the lesion was parenchymatous haemorrhage; in 75 it was an infarct, which was small (< 6 cm3) in 30.5%, moderate sized (6-60 cm3) in 38.6% and large in 30.6%. In the cases of infarct, only the cortisol was significantly different in the three groups (average (DE) standard deviation, respectively: 80.6 (50), 114 (124) and 246 (207); p = 0.0014). This relationship persisted when the cortisol level was compared with the volume in cm3 (p = 0.0028). The cortical infarcts had significantly higher levels of cortisol than the more deeply situated infarcts (83.2 (55) as compared to 174 (184); p = 0.0321), but the latter were smaller and no difference was seen when size was taken into account. All findings were similar in haemorrhages and infarcts of equal size. CONCLUSIONS: There was no relationship between the catecholamines and the type or size of the lesion. In our series, the site of the lesion did not appear to have any effect on the characteristics or intensity of the hormone response.
We describe a women of 22 years of age who had had a vertical gastroplasty (as treatment for morbid obesity). She was admitted to hospital with a 4 week history of nausea and vomiting of food. Treatment with intravenous dextrose, without vitamin supplements was started. One week later she complained of diplopia, paresthesia and weakness of the limbs. All investigations proved to be normal. A deficiency state was suspected, probably Wernicke's encephalopathy, although no alterations were seen in her mental state. We started treatment with high doses of parenteral thiamine, other vitamins and a suitable diet. The treatment was followed by complete recovery. Few neurological complications have been described in association with vertical gastroplasty. The commonest are polyneuropathies. The probable deficiency origin of these is considered. We emphasise the importance of vitamin supplements following the surgical treatment of morbid obesity to avoid the development of deficiency states. Wernicke's encephalopathy is due to thiamine deficiency. It may be associated with any type of malnutrition, not only with chronic alcoholism. The full clinical triad which is diagnostic of this condition is only present in one third of the cases. When the condition is suspected on clinical grounds treatment should be started early to avoid the occurrence of irreversible secuelae.
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We describe an acute-onset, sharp, short-lasting (few seconds) headache at the vertex, that first occurred 10 years ago in a 44-year-old woman. Attacks were triggered by vigorous laughing. A magnetic resonance imaging study showed a Chiari type 1 malformation. To our knowledge, laugh-induced headache with long-term evolution in association with Chiari type 1 malformation has not been previously reported.
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From studies of the incidence of epilepsy, figures of between 40 and 70 per 100,000 inhabitants are obtained whilst in studies of prevalence, 5 to 7 cases per 1,000 are found. Cerebrovascular disease is the commonest cause of epileptic crises in the developed world, being more frequent in patients aged over 60, who make up 50% of all cases. Depending on the moment of presentation of crises in relation to the cerebrovascular disease, these may be classified as herald crises or precursors of vascular epilepsy, early crises if they occur during the first week and late crises if they occur after. Whilst early crises are usually due to metabolic or cytotoxic factors, the late crises occur in true vascular epilepsy. When these patients are assessed it is also important to consider increased hospital mortality in those with early crises and possible deterioration of neurological deficit as sequelae following late epileptic crises.
OBJECTIVE: Peripheral facial paralysis is one of the commonest mononeuropathies. The frequency of idiopathic peripheral paralysis or Bell's palsy varies between 62% and 93% of all cases, with an incidence of between 14 and 25 cases per 100,000 inhabitants per year. However, in spite of its relative frequency in the population, there is still no definite unanimously agreed strategy currently used by neurologists. Although its course is relatively benign, up to 16% of the patients show moderate or severe sequelae according to follow-up data in 1,011 untreated patients. In this article we review the aetiology, diagnostic methods and therapeutical strategies at the present time. DEVELOPMENT: The topographic diagnosis of the lesion is based on the symptoms associated with the paralysis. The neurophysiological studies (trigeminofacial reflection and electroneurogram), usually done after the first week are prognoses that permit differentiation of the degree of the lesion (neuropraxis, axonotmesis or neurotmesis). In spite of recent trials with combined therapy (acyclovir and steroids) the most generally accepted treatment at present is still prednisose at a dose of 1 mg/kg/day. CONCLUSIONS: Peripheral facial paralysis is a common condition, usually with no apparent cause and an eminently clinical diagnosis. The electrophysiological studies determine the prognosis. Currently the standard treatment is still oral prednisone.
OBJECTIVES: To review the differentiating characteristics of symptomatic acute epilepsies, epidemiology, aetiology and controversies over treatment, and describe our experience with symptomatic acute epilepsy in cerebrovascular disorders. DEVELOPMENT AND CONCLUSIONS: The so-called symptomatic acute epilepsies show clearly differentiated characteristics with regard to true epileptic disorders: 1. A clearly identified causal association; 2. Generally tend not to recur; 3. Usually long-term anti-epileptic treatment is not necessary. Therefore the most suitable term for them is symptomatic acute seizures. They make up a large proportion of all newly-diagnosed epilepsies around 40%. The highest incidence occurs during the first year of life (probably because of the high incidence of seizures due to encephalopathies, metabolic disorders and infections) and in elderly patients (especially in relations to cerebrovascular disorders). The commonest causes are: cerebrovascular disorders, head injury, infections of the central nervous system, alcohol and drugs. The risk of subsequent epilepsy is increased in a subgroup of these patients, especially in cases with associated cerebrovascular disorders, head injuries and central nervous system infection. Long-term preventive treatment is rarely indicated in these patients.
INTRODUCTION: Vigabatrin is an effective antiepileptic drug for treatment of partial crises with or without generalization. It acts by increasing GABA levels by irreversible inhibition of the enzyme GABA-transaminase. In recent years there have been several reports published on the appearance of alterations of the visual fields of patients treated with this drug. OBJECTIVE: To study the prevalence and characteristics of the visual field changes associated with vigabatrin treatment in an adult epilepsy clinic. PATIENTS AND METHODS: Ophthalmological examination, consisting of questions about eye symptoms, study of the fundus oculi, Humphrey-type campimetry, protocol 30-2, visual evoked potentials and electroretinogram were done on a group of 10 patients on long-term vigabatrin treatment. RESULTS: Six of the ten patients (60%) had campimetric alterations, which were serious in two cases (20%). Only the two patients with severe field defects complained of sight changes when questioned and their complaints were mainly of repeatedly bumping into things. In two patients (20%) there was pallor of the optic nerve. In both cases, the patients with severe field defects showed alterations on the electroretinogram. Visual evoked potentials were normal in all cases. CONCLUSIONS: There is a very high prevalence of visual field defects in patients on long-term treatment with vigabatrin. Clinical ophthalmological signs are not usually seen until advanced stages. Pallor of the optic nerve was seen in a group of patients. It is very important that serial campimetric studies are done for early detection of such alterations.
OBJECTIVE: The neuropsychological assessment of the epileptic patient is a very important aspect of diagnosis and treatment. It may be used to contribute to localization of the hemisphere involved in the seizures, differentiate situations of anxiety or depression or when planning treatment for rehabilitation. We review the different aspects of neuropsychological changes in patients with epilepsy. DEVELOPMENT: Firstly we review the different tests used in the neuropsychological assessment of epilepsy. Dodrill's neuropsychological battery of tests, in which the patients score less than the controls, is the most commonly used. We then evaluate and study the so-called 'transient cognitive disorder'. We also study memory problems in epilepsy. There may be episodes of seizures with amnesic features ('amnesic epileptic seizures'). Finally, the possibility of neuropsychological dysfunction secondary to antiepileptic drugs should always be considered. CONCLUSIONS: Epileptic patients have lower scores than persons taken as controls for the results of various neuropsychological tests, although there is less difference between the two groups when the patient group is made up of persons with a normal intelligence quotient. Transient cognitive involvement is common in epileptics and may cause underachievement at school or psychological problems. Memory disorders, particularly subjective, are common in epileptics, although neuropsychological tests other than those generally used may be necessary to evaluate this. It is possible that such memory disorders, if occurring as seizures, may be due to amnesic partial crises, which should always be differentiated from the diagnosis of transient global amnesia. Almost all antiepileptic drugs can cause negative neuropsychological effects, especially the benzodiazepines and barbiturates.
OBJECTIVE: To review the current treatment and usefulness of lamotrigine in absence seizures. DEVELOPMENT: Absence seizures are classified amongst the generalized epilepsies. They are defined as a transient loss of consciousness of sudden onset and recovery characteristically associated with generalized spike-and-wave discharges on the EEG. In recent years, the epileptic syndromes associated with this type of seizure have been better defined, basically by means of video-EEG studies. The International League Against Epilepsy has recognized four epileptic syndromes with typical absences: absence-epilepsy of childhood, juvenile absence-epilepsy, juvenile myoclonic epilepsy and epilepsy with myoclonic absences. The classical treatment for this type of seizure was based on ethosuximide, or more often, sodium valproate. Sometimes both drugs together were necessary. Other useful drugs are the benzodiazepines such as clobazam. CONCLUSIONS: We review studies of the efficacy and tolerance of lamotrigine in the treatment of absence seizures, one of the groups of seizures in which this drug has been shown to be most effective. Although studies comparing lamotrigine, valproate and ethosuximide are necessary, we emphasize the possibility that lamotrigine may be a drug of choice in absence seizures.