Biomedical subjects

M Noya

Publications and source records attributed to M Noya.

At least 37 records · Page 2Linked to original sources

PubMed1997

[Concept, classification and pathophysiology of status epilepticus].

Status epilepticus (prolonged or repetitive seizures without a period of recovery between them) is a life-threatening medical emergency for which appropriate diagnosis and treatment are imperative. It is usually classified with a practical aim as convulsive and non-convulsive, generalized and partial. In convulsive status there is a critical period of 30 min before irreversible metabolic alterations appear. The factors that influence the beginning and endpoint of a status epilepticus are unknown but a role has been proposed for both glutamate mediates excitation and lack of GABA mediated inhibition.

Brain↗

PubMed1996

Adherence and invasive capacities of the fish pathogen Pasteurella piscicida.

Pasteurella piscicida strains were weakly or moderately adherent to cell lines, the levels of attachment being variable depending on the cells employed. All the isolates exhibited the highest binding capacity to CHSE-214 cells. Adhesive capacities were affected by heat and sugars but not by proteinase K or by treatment with antisera raised against the lipopolysaccharides of P. piscicida, implicating components of glycoprotein(s) as ligands in the adhesion process. The isolates showed a great binding capacity to intestines from the marine fish hosts gilthead sea bream, sea bass and turbot, with values ranging from 10(4) to 10(5) bacteria/g. Although the P. piscicida strains showed a weak invasiveness in the poikilothermic cell lines employed as in vitro model, the bacteria remained viable inside the infected cells at least for 2 days. The invasion process was inhibited by cytochalasin D indicating the active participation of the host cytoskeleton in the internalization of P. piscicida.

Animals↗

PubMed1996

Cerebrospinal fluid tyrosine and 3,4-dihydroxyphenylacetic acid levels in migraine patients.

We studied biochemical parameters related with central dopaminergic neurotransmission in migraine patients during crisis. We determined tyrosine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in cerebrospinal fluid (CSF) of 47 patients, 29 suffering migraine without aura and 18 suffering migraine with aura, comparing them with 27 control subjects. Tyrosine levels did not differ significantly between patients and controls. The CSF concentration of DOPAC was 0.73 +/- 0.55 ng/ml in the control population, 3.84 +/- 2.08 ng/ml in patients with migraine without aura and 3.30 +/- 1.49 ng/ml in patients suffering migraine with aura. The concentration of DOPAC correlated positively with the intensity of headache. These results suggest that patients with migraine have a central dopaminergic hyperfunction, probably related to a coexisting central dysfunction of noradrenergic neurotransmission.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1996

Neuroexcitatory amino acids and their relation to infarct size and neurological deficit in ischemic stroke.

BACKGROUND AND PURPOSE: The participation of excitatory amino acids (EAAs) in the pathogenesis of ischemic neuronal lesion has been experimentally demonstrated, but clinical experience is scarce. Our objective was to examine EAA levels during the acute phase of cerebral infarction in relation to infarct size and intensity of neurological deficit. METHODS: Using high-performance liquid chromatography, we determined the glutamate, aspartate, taurine, and glycine concentrations in the plasma and cerebrospinal fluid (CSF) of 128 patients with ischemic cerebral infarction confirmed by CT and 43 control subjects. Blood and CSF samples were obtained on admission within the first 24 hours from symptom onset. The severity of the neurological deficit was assessed with the Canadian Stroke Scale immediately after these tests and at 48 hours after inclusion in the study. Infarct volume was determined in a second CT performed between the 4th and 7th day after the patient's inclusion. RESULTS: The concentration of plasmatic glutamate was 121.39 +/- 80.89 mumol/L in the control group and 163.71 +/- 103.13 mumol/L in the patient group (P = .015); in CSF it was 3.46 +/- 1.20 mumol/L in control subjects and 6.55 +/- 4.65 mumol/L in patients (P < .0001). The concentration of glycine in plasma was 158.02 +/- 32.15 mumol/L in control subjects and 189.37 +/- 74.04 mumol/L in patients (P = .007); in CSF it was 6.18 +/- 2.28 mumol/L in control subjects and 11.23 +/- 6.96 mumol/L in patients (P < .0001). The concentrations of glutamate in plasma and in CSF were significantly higher in patients with large cerebral infarcts and in those with cortical infarcts. Levels of glutamate and glycine in plasma and CSF were significantly higher in patients with a higher degree of neurological deficit. CONCLUSIONS: Our results support the excitotoxic activity of glutamate and glycine in patients with cerebral infarction.

Adult↗

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↗

PubMed1996

[The prognostic value and evolution of blood pressure during an acute phase of stroke].

We studied the prognostic influence and evolution of blood pressure during the acute phase of stroke in 89 patients (50 men and 39 women) with an average age of 69.4 +/- 10.8 years. Seventy-two were diagnosed as having ischaemic infarct and 17 as having spontaneous intracerebral haemorrhage. Blood pressure was taken every four hours for twelve days. Clinical situation was evaluated using the Rankin scale. Systolic and diastolic blood pressure progressively decreased without needing any medication in the first two weeks of evolution. The decrease was greatest in hypertense patients and in those with left ventricle hypertrophy. We found the initial figures for systolic and diastolic blood pressure significantly higher in those patients with brain infarct who had not died and in those in a better functional position the second week of evolution. Blood pressure did not influence the prognosis of intracerebral haemorrhage patients.

Acute Disease↗

PubMed1996

[3 year survival in patients hospitalized for acute cerebrovascular disorders].

For three years we studied the mortality and functional situation of all patients admitted in 1991 to the Neurology Service suffering from acute stroke with the exception of subarachnoid haemorrhage cases. We analyzed the cause of death whether directly related to the initial illness or not. Out of 134 patients admitted for acute stroke, 48 (41.02% of the 117 patients examined after excluding 17 whom we did not obtain complete information from) had died after three years. The main causes of death were directly related to acute stroke (37.5%) and pneumonia (37.5%). Death occurred mainly in the first month (79.16% of deaths). Predictive variables for mortality directly related to acute stroke during the first month include severe weakness, brain haemorrhage, dysphasia and earlier incidence of acute stroke. Variables related to higher mortality rate due to other causes in the first month were dysphasia, age and angina antecedents, whereas earlier incidence of acute stroke was associated with a lesser mortality rate for these causes, as distinct from acute stroke itself. Greater levels of weakness and sphincteral incontinence are the best predictive signs of dependency functional situation at the end of the first month and, along with diabetes, after one and three years.

Acute Disease↗

PubMed1996

[A preliminary study of low dosage zuclopenthixol depot in Alzheimer's disease].

Persistent psychomotor agitation and psychotic ideation in patients with Alzheimer's disease are normally treated orally with antipsychotic drugs and are occasionally treated with other drugs. Neuroleptics administered intramuscularly at very low doses are an alternative, especially when the patient rejects medicine as a results of his or her anosognosia or of paranoid manifestations. We present the results we obtained after observing the effects of depot zuclopenthixol in six patients with probable Alzheimer's disease (based upon NINCDS-ADRDA criteria). Psychic abnormalities were assessed as per the Brief Psychiatric Rating Scale (BPRS), the Scale for the Assessment of Positive Symptoms (SAPS) and the Scale for the Assessment of Negative Symptoms (SANS). Possible extrapyramidal side effects were evaluated by means of the Abnormal Involuntary Movement Scale (AIMS). Initially 60 mg (0.3 ml) were administered intramuscularly and successive doses could be modified by +/-20 mg (0.1 ml) according to results seen on the various scales. During the first six weeks of treatment progressive improvement was noted on all three psychic functions scales in all patients. Between the sixth and twelfth weeks improvement continued although without significant change. The AIMS did not show significant changes in the twelve weeks of follow-up. We consider depot zuclopenthixol at low doses as efficacious in treating persistent psychomotor agitation and/or psychotic manifestations of Alzheimer's disease. No undesired side effects were observed in our group after a twelve week follow-up.

Aged↗

PubMed1996

[Experience with pupil tropicamide test in Alzheimer's disease].

Scinto et al (Science 1994; 266: 1051-4) observed that a single drop of 0.01% tropicamide elicited more than a 13% pupil dilatation in 19 individuals with probable or possible Alzheimer's disease (AD) and 3 cognitive abnormal elderly without dementia, but not in 30 out of 32 normal elderly and 3 out of 4 patients suffering from other dementias. It could be an easy and bloodless test to help in diagnosing AD. We have administered the same test to 10 patients with probable AD (NINCDS-ADRDA criteria) and twenty 40-90 year-old control subjects (10 of whom were sons or daughters of AD patients and 10 without a family history of dementia). The researcher does not know which group the subject belongs to. He administers a single drop of 0.01% tropicamide in eye and one drop of 0.45% normal saline solution in the other (without knowing the contents of either vial) and measures the pupil diameter by means of a Goldmann pupilometer in basal condition and 10, 15, 25, 30, 35, 45, and 55 minutes after. The results show that it is necessary to measure the pupils at least between the minutes 25 and 55 to detect tha maximum pupil dilation in every case. The cutoff point to consider the result positive must be located between 43 and 50%. If we establish the cutoff point in 50% of pupil dilation, 90% of AD patients and 35% of control subjects show a positive response. There was not a statistically significant difference between both control groups. Our results from this test show a sensitivity of 90% and a specificity of 65%. The positive responses of some control subjects may express a weak specificity, or perhaps they mean that we have a marker of the pre-clinical stage of the disease before us.

Adult↗

PubMed1996

Morphology and histochemistry of a PAS-positive granular cell in the gills of the gilthead seabream, Sparus aurata L.

A periodic acid-Schiff-positive granular cell (PAS-G cell) was investigated by light and electron microscopy in the gills of the gilthead seabream (Sparus aurata L.). Despite the use of several fixatives, it was only possible to demonstrate metachromasia after fixing these cells with a solution of 10% formol and 5% acetic acid in methanol. Using this fixative, their granules stained purple with toluidine blue or thionin. In semithin resin sections, the granules also stained purple with toluidine blue-borax. Ultrastructurally, these cells possessed 2 types of homogeneous electron-dense granules and characteristic long thin surface processes resembling a string of beads. These PAS-G cell share morphological features with basophils and mast cells, and were metachromatic. They were observed in sites similar to those for mast cells in mammals.

Aminosalicylic Acid↗

PubMed1996

[Differential diagnosis of the epilepsies].

Epileptic seizures result from excessive neuronal discharge. The diagnosis of epilepsy, defined as spontaneously recurrent seizures, is mainly clinical. The possibility that a patient is experiencing other acute cerebral events, such as syncope or pseudoseizures, must always be considered. Electroencephalography is an important diagnostic aid that facilitates the classification of epilepsies. Magnetic resonance and computerized tomography make it feasible to investigate possible etologies, while functional neuroimaging studies, such as simple photon emission computed tomography and positron emission tomography afford information on the origin of neuronal discharge. Whether or not an epileptic seizure is likely to form part of a specific epileptic syndrome must be assessed, given the therapeutic and prognostic consequences. The diagnosis of epileptic patients must be based on medical history and physical examination.

Adolescent↗

PubMed1995

Genetic markers: association study in migraine.

Eleven genetic markers were typed in 112 unrelated patients with migraine (50 with aura, 62 without aura) and compared with a random sample of healthy individuals. No significant differences were found for the ABO and Rh systems, acid phosphatase 1, phosphoglucomutase 1, adenosine deaminase, haptoglobin, transferrin, alpha-1-antitrypsin, and D1S80. Strong associations between the group of patients with migraine and group-specific component GC 1F-1F and esterase-D ESD 2-2 phenotypes were observed. These associations raise the possibility that a molecular genetic factor for migraine may exist in or near the Group Component (chromosome 4) and Esterase D (chromosome 13) loci, and represent a first comprehensive step in the eventual localization and isolation of the migraine genes.

Adolescent↗

PubMed1995

Amino acid transmitters in patients with headache during the acute phase of cerebrovascular ischemic disease.

BACKGROUND AND PURPOSE: The pathophysiology of headache occurring at stroke onset is unknown. Migraine and ischemia share an excessive release of neuroexcitatory amino acids. Inhibitory amino acids also may be implicated in both diseases. We investigated whether fluctuations of these amino acids occur in headache accompanying cerebral infarction. METHODS: We studied 100 patients with infarction in the territory of the middle cerebral artery. Neurological impairment was assessed using the Canadian Neurological Scale and Barthel Index. Size of infarction was determined with CT. Twenty-eight patients developed headache. Glutamate, aspartate, and taurine were quantified in blood and cerebrospinal fluid (CSF) within 24 hours of stroke onset with cationic exchange chromatography. RESULTS: Stroke subtypes, size of infarct on CT, and clinical scales were similar in patients with and without headache. Plasma glutamate level was 321.14 +/- 149.53 mumol/L in patients with headache and 233 +/- 107.23 mumol/L in those without headache (P < .005). Glutamate in CSF was higher in patients with headache (4.6 +/- 1.49 mumol/L) than in patients without headache (3.11 +/- 1.18 mumol/L) (P < .001). Aspartate concentrations in plasma and CSF were similar in both groups. Taurine concentrations in plasma were 103.10 +/- 52.82 mumol/L and 177.49 +/- 90.92 mumol/L in headache and nonheadache patients, respectively (P < .001). Taurine levels in CSF were 5.42 +/- 2.42 mumol/L in patients with headache and 9.27 +/- 5.31 mumol/L in those without headache (P < .001). No significant correlation was found between amino acid levels in plasma or CSF and size of infarction. CONCLUSIONS: Amino acid neurotransmitters play a role in the pathophysiology of headache that occurs at the onset of stroke. The ischemic penumbral area, more than the infarction itself, may cause a state of cortical hyperexcitability that would be responsible for the cortical release of amino acids and the induction of headache by altering pain perception mechanisms.

Adult↗

PubMed1995