[The clinical picture of migraine].
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Biomedical subjects
Publications and source records attributed to M Noya.
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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.
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.
We present the principal differential characteristics of neuralgia of symptomatic and idiopathic trigeminus. Out of 39 consecutive patients with neuralgia of trigeminus evaluated clinically and with neuroimage study, we find recognizable pathology in 10 (3 arterio-venous malformations, 1 dolichoestasia of basilar artery, 3 tumors, 3 multiple sclerosis). Symptomatic neuralgia occurs in patients with lower average age and is accompanied by atypical symptoms or abnormal neurological signs and is no different from idiopathy as a response to pain from medical treatment. Painful affectation of the trigeminus requires the realization of complementary explorations aiming to dismiss associated neurological pathology.
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.
The MR findings in 27 patients with myotonic dystrophy were compared with those observed in 11 patients with other muscular dystrophies: six with limb-girdle dystrophy, three with facioscapulohumeral muscular dystrophy and two with Becker-type muscular dystrophy. Clinical status was graded into 10 stages. The MR study was performed at the medium third of the thigh, with a slice thickness of 7.5 mm (TR: 750/TE: 25 for T1; TR: 2200/TE: 30/90 for DP/T2). Muscle signal intensity was evaluated with a four-point grading scale using subcutaneous fat as a reference. Statistical analysis was done using the Mann-Whitney-Wilcoxon's test and simple linear regression. In the myotonic dystrophy group, 81.4% of the patients showed an abnormal signal at the crural muscle level, adopting a semilunar shape around the anteroexternal side of the femur. The presence and intensity of this hyperintense signal correlated positively with the duration of disease (r = 0.54) and the clinical stage (r = 0.69). Of the 11 patients with other muscular dystrophies, only three (27.2%) showed hyperintense signal at the crural muscle level. MR imaging of patients with muscle disease may contribute to the in vivo study of muscular dystrophy, its differential diagnosis and the detection of asymptomatic patients.
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.
We measured platelet-rich plasma (PRP) serotonin in patients suffering from tension-type headache, before and after treatment with amitriptyline, comparing them with a healthy control group and patients with untreated depression. We evaluated the severity of headache and depression in each group. PRP serotonin levels were higher in patients with headache than in controls and depressed patients. We observed a fall of PRP serotonin in patients with tension-type headache to similar levels after treatment as the depressed group. This fall was correlated with the improvement of headache but not with depression scales. Our data suggest that the rise of platelet serotonin levels in tension-type headache is related to pain and not depression.
Taurine is the amino acid with the highest concentration in the human body. Its physiologic functions are not yet well understood. As a neurotransmitter or neuromodulator it may display inhibitory functions. We have measured taurine levels in plasma and cerebrospinal fluid of migraine patients during attacks, comparing them with controls. Patients with migraine had significantly higher concentrations than controls. No sex or age influence over the amino acid levels were observed. Plasma taurine levels in patients with classic migraine correlated negatively with severity of headache. Central taurine liberation during migraine crisis may be due to spontaneous depolarization or a defensive reaction in the context of cerebral homeostatic processes.
There is clinical and pharmacological evidence of the existence of sympathetic dysfunction in migraine. Adrenaline and noradrenaline concentrations were determined in plasma and CSF of patients during attacks of common or classic migraine, comparing them with controls suffering from stress. Plasma noradrenaline levels were significantly lower in the patients with common migraine than in controls (p < 0.05). Other catecholamine levels in plasma and CSF in both migraine groups were only slightly lower than in controls. Our results suggest that central sympathetic dysfunction exists in patients with migraine.
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We report a 31 year old patient with cerebrotendinous xanthomatosis who presented with dementia, tendinous xanthomas, cataracts, pyramidal involvement, cerebellar ataxia and peripheral neuropathy. Cerebral CT scan demonstrated diffuse hypodensity in the white matter in both cerebellar hemispheres while MR detected additional focal alterations in both frontal lobes. MR study of the Achilles tendon showed a diffuse enlargement of the tendon with multiple areas of hypersignals in T1 and T2 demonstrative of the lipid deposits, interpossed between the isosignal zones that may correspond to the inflammatory reaction secondary to the accumulation of cholesterol and cholestanol.
The transitory suppression of L-dopa in patients with advanced Parkinson's disease improves motor response upon reintroduction of the drug although this improvement is not constant. The degree and duration of clinical improvement obtained following L-dopa drug holiday were studied and the factors which may intervene in the result of 32 patients with Parkinson's disease were analyzed. Improvement was found in 100% (24.9 +/- 6.7%) with significant differences being observed in the degree of disability (p < 0.05) and the final decrease of the doses of L-dopa (p < 0.05). Improvement was maintained during 10.3 +/- 7.9 weeks. Linear regression studies did not show any relation between the length of the drug holiday, longer than 4 days, and the degree and maintenance of improvement or final decrease of the doses of L-dopa. The authors consider this procedure useful in patients with important fluctuations in treatment response or with important refractory side effects to other measures.
The observation of an abscess in the brain stem and cerebellum due to Listeria monocytogenes is presented. The patient was a 55 year old diabetic, alcoholic, gastrectomized male in whom a febrile and meningeal syndrome developed. Three days later he had a progressive unilateral dysfunction of the cranial nerves. The cerebrospinal fluid showed pleocytosis of the polymorphonuclear cells, an increase in proteins and low glucose in relation with the glycemia. No parenchymatous lesion was observed upon emergency computerized tomography. Magnetic resonance imaging showed a hyper-signal lesion in the brain stem and cerebellum with a contrast enhancement in ring. Following antibiotic treatment the clinical evolution of the patient was favorable with slight focal sequelae persistent at discharge. A review of the epidemiology, clinical manifestations and treatment of this infection is carried out.
Seven biological markers were studied in a population of 236 patients (144 females, 92 males) with multiple sclerosis as was the relation with the different degrees of diagnostic certainty (Rose and Poser scales), the time of evolution and number of bouts of the disease. The IgG concentrations, IgG ratio and the quantification of the intrathecal IgG synthesis by the Tourtellotte formula isolatedly constituted the most sensitive biological markers for the diagnosis of multiple sclerosis. Altogether, the determination of the number of cells, IgG and the IgG ratio achieved diagnostic sensitivity of 94% for defined multiple sclerosis. The IgG ratio was the most closely related biological marker related with the number of bouts and the time of evolution of the disease.
The relation between the results of 7 biological markers (cells, total protein, albumin, IgG, IgG ratio, Tibbling ratio, and Tourtellotte's formula) and 4 paraclinical tests (PEV, PEATC, CT and MR) in 236 patients with multiple sclerosis (MS) not selected by the localization of symptoms were studied. One hundred forty-one had clinically defined MS, 22 had defined MS supported by a laboratory and 68 had clinically probable MS. The existence of a relation between PEV and MRI abnormality and the increase in the concentration and the ratios of intrathecal IgG synthesis and the degree of certainty of disease diagnosis was demonstrated. The most sensitive test was MRI (93%) followed by VEP (83%) and BAEP (60%) and the sensitivity of the study with high resolution CT including 59 patients explored by double enhancement and delayed cut off was very low (33%). It was considered that for the lack of a specific diagnostic test the use of biological markers PEV and MR constituted a necessary aid in the diagnosis of MS.
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