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R Leira

Publications and source records attributed to R Leira.

At least 19 recordsLinked to original sources
PubMed2001

Predictors of deteriorating cerebral infarct: role of inflammatory mechanisms. Would its early treatment be useful?

The development of neurological deterioration in the hours following the stroke onset occurs in somewhat more than 1 in 3 cerebral infarcts and is associated with an increase in morbidity and mortality. This early deterioration (0--48/72 h) entails the conversion of the ischemic penumbra area in an irreversible lesion, a process that is mediated as much by hemodynamic changes in the local cerebral circulation as by biochemical mechanisms. Late neurological deterioration (3--7 days) is more frequently associated with systemic causes. Knowledge of the various clinical, biochemical and imaging markers associated with neurological deterioration is consequently of fundamental importance. For their repercussion in clinical practice, we classify these predictors of deteriorating cerebral infarct into nonmodifiable, modifiable and possibly modifiable. The reduction in cerebral blood flow in a particular cerebral zone causes very early cerebral damage as a consequence of a significant liberation of neuroexcitatory amino acids, followed by an excessive entry of calcium into the interior of cells; this process causes lipid peroxidation, disintegration of the cellular membranes, nuclear destruction and neuronal death. Moreover, ischemia and posterior reperfusion induce an inflammatory response leading to further cellular destruction. It is therefore conceivable that therapeutic interventions aimed at decreasing proinflammatory cytokines and cell adhesion molecules might result in better outcome in this population.

Cerebral Infarction↗
PubMed2001

Neurological deterioration in acute lacunar infarctions: the role of excitatory and inhibitory neurotransmitters.

BACKGROUND AND PURPOSE: The mechanisms involved in the neurological deterioration of acute lacunar strokes are unknown. Although accumulating evidence suggests that glutamate release plays a role in the progression of territorial infarctions, it remains to be established whether excitotoxicity also participates in lacunar stroke progression. We investigated whether excitatory and inhibitory amino acid concentrations in blood predict subsequent progressive motor deficits in lacunar infarctions. METHODS: We studied 113 consecutive patients with lacunar infarct, defined by clinical and computed tomography/magnetic resonance imaging criteria, within the first 24 hours after stroke onset. Neurological deterioration was defined as a decrease of >/=1 points in the motor items of the Canadian Stroke Scale in the first 48 hours after admission. Glutamate, glycine, and GABA were determined by high-performance liquid chromatography in plasma samples obtained on admission. Predictive values, sensitivity, specificity, and accuracy of specific glutamate and GABA concentrations and glutamatexglycine/GABA index for progression of lacunar stroke were calculated. RESULTS: Twenty-seven patients (23.9%) had neurological worsening. Plasma concentrations of glutamate (253+/-70 versus 123+/-73 micromol/L, mean+/-SD) were higher and those of GABA (140+/-63 versus 411+/-97 nmol/L) were lower in the progressing group than in the nonprogressing group (both P<0.001). Glutamate concentrations >200 micromol/L and GABA levels <240 nmol/L had a positive predictive value for neurological deterioration of 67% and 84%, respectively. A excitotoxic index >106 had a positive predictive value of 85%. CONCLUSIONS: These findings suggest that an imbalance between the glutamate and GABA concentrations may play a role in the pathophysiology of progressing lacunar infarctions.

Acute Disease↗
PubMed2000

[Rizatriptan].

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Dose-Response Relationship, Drug↗
PubMed1999

[Spanish study of quality of life in migraine (II). Profile of medication consumption and subjective efficacy].

OBJECTIVES: The response to the different antimigraine medications is variable. In this study we have analysed the profile of prescription of these antimigraine medications, both preventive and symptomatic, by a group of spanish neurologists and examined the subjective efficacy of these compounds. PATIENTS AND METHODS: Neurologists from 7 hospitals in different spanish regions interviewed 305 patients (at least 40 per hospital) who met migraine diagnostic criteria. They used an ad hoc questionnaire in which the antimigraine medications, both symptomatic and preventive, taken by the patients, as well as their subjective response were registered. Patients with transformed migraine or tension-type headache more than 2 days per week were excluded. RESULTS: Analgesics, non-steroidal anti-inflammatory drugs, ergotics and sumatriptan had been taken by 99, 69, 54 and 40% of the 305 interviewed patients, respectively. A subjective good response was refered to by 9% of patients who had taken analgesics, 23% of patients who had taken non-steroidal anti-inflammatory drugs, 39% of those who had taken ergotics and 63% of patients with sumatriptan. The current symptomatic treatment was: analgesics 34% of cases, non-steroidal anti-inflamatory drugs 26%, ergotics 13% and sumatriptan 63%. Regarding preventive treatments, 108 patients (35%) had been treated with calcium-antagonists, 87 (29%) with beta-blockers, 55 (18%) with amitriptyline and only 7 (2.2%) with valproic acid. The percentages of good responses to these drugs were: 55% for beta-blockers, 42% for calcium-antagonists and 31% for amitriptyline. CONCLUSIONS: Our data confirm that analgesics are not efficacious in the majority of migraine patients and that the advent of sumatriptan has clearly improved the quality of migrane symptomatic treatment, even though about one-third of migraine patients do not respond to this drug. This study confirm that calcium-antagonists are the antimigraine preventive treatment most frequently prescribed in our country, even though their subjective efficacy is lower than that of beta-blockers.

Analgesics, Non-Narcotic↗
PubMed1998

[Clinical efficacy of zolmitriptan in migraine].

Zolmitriptan (previously known as 311C90) is a serotoninergic 5-HT1B/D agonist with high oral bioavailability with a double, central and peripheral, action mechanism. Evaluation of its clinical efficacy was developed in a program of clinical studies (search and confirmation of dosis, comparative and long term studies) and through analysis of efficacy in different clinical situations. Zolmitriptan shows a high effectiveness in the treatment of migraine crisis, significantly reduces the headaches by 2 hours of its administration, reduce the symptoms associated with migraine (nausea, photophobia and phonophobia) and improves the quality of life of the migraine patient. The efficacy is independent of the type of migraine characteristics of the patient as well as of the administration of other concomitant medications. The dosis of 2.5 mg of zolmitriptan has been found to be the optimum considering both efficacy and tolerability.

Adolescent↗
PubMed1997

Pseudomigraine with temporary neurological symptoms and lymphocytic pleocytosis. A report of 50 cases.

This is the first large series, comprising 50 patients who suffered a total of 164 episodes, of pseudomigraine with temporary neurological symptoms and lymphocytic pleocytosis (PMP syndrome). Onset of PMP was between the ages of 14 and 39 years and was most frequent in males (68%). Eight males (24%) and five females (31%) had a personal history of migraine. One-quarter had had a viral-like illness up to 3 weeks prior to the onset of the syndrome. The clinical picture consisted of one to 12 episodes of changing variable neurological deficits accompanied by moderate-to-severe headache and occasionally fever. The headaches were described as predominantly throbbing and bilateral with variable duration (mean, 19 h). The mean duration of the transient neurological deficits was 5 h. Sensory symptoms were most common (78% of episodes), followed by aphasic (66%) and motor (56%) symptoms. Visual symptoms appeared in only 12% of episodes. The most frequent combinations were motor aphasia plus sensory and motor right hemibody symptoms (19% of episodes), motor aphasia plus right sensory symptoms (10%) and isolated right (9%) or left (9%) sensory symptoms. All patients were asymptomatic between episodes and following the symptomatic period (maximum duration 49 days). Lymphocytic pleocytosis ranged from 10 to 760 lymphocytic cells/mm3 CSF (mean, 199). In CSF, protein was increased in 96% of patients, IgG was normal in 80% of cases and oligoclonal bands were not found. Adensoine deaminase values were slightly above normal in two out of 16 patients tested. Extensive microbiological determinations, including viral HIV and borrelia serologies, were negative. Brain CT and MRI were always within normal limits, while EEG frequently showed focal slowing. Conventional cranial angiography was performed on 12 patients. In only one were there abnormalities suggestive of localized vascular inflammation, coincident with the focal neurological symptoms. Two patients developed PMP symptoms immediately after angiography. SPECT, performed on only three patients in the symptomatic period, revealed focal areas of decreased uptake consistent with the clinical symptoms. PMP aetiology remains a mystery; chronic arachnoiditis, viral meningoencephalitis or migraine are not plausible aetiological explanations. Because a number of patients had had a prodromic viral-like illness, we hypothesize here that such a viral infection could activate the immune system, thereby producing antibodies that would induce an aseptic inflammation of the leptomeningeal vasculature, possibly accounting for this clinical picture.

Adolescent↗
PubMed1997

[Migraine due to infarct].

Migraine is a risk factor for cerebral stroke, particularly in young women. Whether the migrainous process is a triggering or contributing factor in the ischemic profile, or is the sole cause of stroke, is impossible to establish with certainty. Epidemiological, pathophysiological and clinical evidence are in no way conclusive. The symptoms and lesions of migrainous stroke suggest the involvement of a mechanism similar to that of migrainous aura, although the infarction process is of greater intensity and lasts longer. Migrainous stroke should be considered an evolutionary complication of aura. Thus, the best treatment consists of adequate control of migraine attacks with the reduction of frequency, intensity and duration. The avoidance of migraine drugs with marked vasoconstrictive action, and the removal of other vascular risk factors (smoking and oral contraceptives) are additional measures for the prevention of migrainous stroke.

Adult↗
PubMed1996

[Diet and migraine].

Some foods in our diet can spark off migraine attacks in susceptible individuals. Some foods can bring an attack on through an allergic reaction. A certain number such as citrus fruits, tea, coffee, pork, chocolate, milk, nuts, vegetables and cola drinks have been cited as possible allergens associated with migraine. This mechanism has however been criticized: an improvement in symptoms by eliminating some food(s) from our diet does not necessarily mean an immunologically based allergic reaction. The high IgE incidence rate is not greater in such patients than in the population at large. Other allergic reactions unrelated to diet may also be associated with migraine attacks. On the other hand substances in food may be the cause of modifications in vascular tone and bring migraine on in those so prone. Among such substances are tyramine, phenylalanine, phenolic flavonoids, alcohol, food additives (sodium nitrate, monosodium glutamate, aspartame) and caffeine. Another recognized trigger for migraine is hypoglycemia. Such foods as chocolate, cheese, citrus fruits, bananas, nuts, 'cured' meats, dairy products, cereals, beans, hot dogs, pizza, food additives (sodium nitrate, monosodium glutamate in Chinese restaurant food, aspartame as a sweetener), coffee, tea, cola drinks, alcoholic drinks such as red wine, beer or whisky distilled in copper stills, all may bring on a migraine attack. For every patient we have to assess which foodstuffs are involved in the attack (not necessarily produced by consuming the product concerned) in order to try to avoid their consumptions as a means of prophylaxis for migraine.

Diet↗
PubMed1996

[Cerebral hemorrhage and migraine].

The connection between migraine and brain haemorrhage is controversial. We present the case of eight nonhypertense patients all aged under 57 with migraine antecedents who suffered brain haemorrhage during an attack. All underwent analytical study, chest X-ray, electrocardiography, computerized tomography scan and brain panangiography. The study was completed in six cases with an immunological analysis and in a further five with brain magnetic resonance. Seven patients habitually took vasoactive drugs to relieve migraine. The results do not show any other cause of brain haemorrhage. It is possible haemorrhage may be related to vascular lesion brought about by ischaemia secondary to vasospasms.

Adolescent↗
PubMed1994

Plasma monoamines in tension-type headache.

Clinical and pharmacological data suggest a derangement of central monoaminergic systems in tension-type headache. Biochemical evidence has been rarely recognized. These findings may relate with pathophysiological mechanisms of headache or with underlying depression. We measured platelet-rich plasma serotonin and plasma catecholamines (norepinephrine, epinephrine, and dopamine) in 30 patients with tension-type headache and in 20 healthy controls, using High-Pressure Liquid Chromatography. We studied differences between groups and the relation between biochemical parameters and clinical indices evaluating duration and severity of headache and depression. Platelet serotonin levels in tension headache patients were higher than in controls (P < 0.001). Plasma catecholamine levels were lower in patients than in controls (P < 0.001 for epinephrine and dopamine, and P < 0.05 for norepinephrine). There was a positive correlation between dopamine levels and duration of history of headache (r = 0.55, P < 0.05). A negative correlation between epinephrine levels and severity of headache was observed (r = 51, P < 0.01). No correlations were found between monoamine levels and severity of depression. Our results add to the evidence of alterations of monoaminergic central systems in tension-type headache patients. These alterations seem to be independent from the underlying depression and related to the pathophysiologic mechanisms of headache.

Adult↗
PubMed1994

[Prognostic factors in spontaneous intracerebral hemorrhage].

The introduction of etiological, diagnostic and therapeutical factors have modified the knowledge on the evolutive behaviour of spontaneous intracerebral hemorrhages (ICH). Mortality and morbidity associated to spontaneous ICH were assessed using as independent variables clinical and neuroimage factors obtained upon admission of the patients. We studied 228 patients with spontaneous ICH selected from a data bank of 277 patients with non-traumatic ICH. During the first 24 hours, we assessed several clinical factors (arterial hypertension, Glasgows Neurological Scale and Barthels Scale) and TC images (size, location, extension of bleeding to ventricles, edema and atrophy). Thirty-one per cent of the patients died during the first 2 months. The multiple linear regression study showed that mortality was related to variables of the Glasgows Neurological Scale upon admission, extension to ventricles, size of ICH and perilesional edema, whereas the morbidity was only related to the size of the hemorrhage. Severity of the clinical affection, extension of the bleeding to ventricles, size of the hemorrhage and presence of perilesional edema, but not arterial hypertension, were the main factors affecting mortality at two months of spontaneous ICH.

Adolescent↗
PubMed1994

[Changes in neuroexcitatory amino acids during and between migraine attacks].

We studied changes in plasma levels of neuroexcitatory amino acids during and between migraine attacks in 16 patients with migraine without aura, 11 with aura and 21 controls. Glutamic acid levels between attacks were 1.027 +/- 0.60 and 0.890 +/- 0.41 mg/dl in migraine patients without and with aura, respectively; during attacks the levels were 0.535 +/- 0.23 and 0.601 +/- 0.20 for the same patients. The concentration of glutamic acid in the control group was 0.980 +/- 0.64 mg/dl. Aspartic acid levels between attacks in patients without and with aura were 0.179 +/- 0.04 and 0.167 +/- 0.03 mg/dl. Concentrations during attacks were 0.129 +/- 0.02 and 0.119 +/- 0.02 mg/dl for the same patients. Plasma levels of aspartic acid for controls were 0.146 +/- 0.03 mg/dl. We found no significant variations in neuroexcitatory amino acids between migraine attacks in patients with an without aura; changes took place only during attacks, possibly related to the mechanisms of the spreading depression process.

Adult↗
PubMed1993

Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks.

A current hypothesis for migraine suggests that neuroexcitatory amino acids may participate in the triggering of attacks. To investigate this possibility we measured glutamic and aspartic acid level in plasma and cerebrospinal fluid (CSF) of patients with common and classic migraine during attacks, making comparisons with controls suffering stress. Plasma levels of amino acids in migraine patients were lower than in controls. CSF concentrations of glutamic acid were higher in migraineurs than in controls. Our results suggest an excess of neuroexcitatory amino acids in the CNS of migraine patients during attacks, possibly favoring a state of neuronal hyperexcitability.

Adult↗