[Unstable angina in relationship to intake of zolmitriptan].
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Biomedical subjects
Publications and source records attributed to E Corredera.
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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.
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.
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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.
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.
PURPOSE: To compare the diagnostic yield of CT scan and perfusion SPECT on admission and its prognostic value in clinical outcome. METHODS: 25 ischemic stroke cases were studied on admission (<24 h) and at 30-60 days by CT scan, 99mTc-HMPAO-SPECT and neurological scales. Infarct size and severity on SPECT were assessed: visually "Total Weighted Score," added value in 22 areas, and by several semiquantitative count-based indices. RESULTS: Sensitivity: the first CT scan was positive in 24% patients, initial SPECT in 75% (73% of pure subcortical infarcts and 91% of those with cortical involvement). Localization: kappa: 0.725 between SPECT findings on admission and those in control-CT at 5 days. Extent and severity: correlations between count-based and visual indices (r: >0.719), the latter correlated slightly better with clinical scales. Both predicted similarly (Rho>0.739) infarct size in CT diagnostic scan. Early Outcome: There were statistical differences between deceased and survivors in SPECT (<24h) indices and CT-infarct size (mean 5 days), but not in neurological scores on admission. Long term Outcome: Correlation of initial SPECT indices with follow-up functional scores (SNSLP, Barthel index; mean 37 days) was only significant for visual SPECT indices (Rho:0.560 to 0.620). Nevertheless the best predictor of functional status on discharge was the Barthel Index on admission. CONCLUSIONS: 1) Early SPECT has good sensitivity and accurate infarct size prediction so it can be a useful tool for deciding thrombolytic therapy; 2) Visual scores perform as well as more complex indices; 3) Infarct volume seems to be a critical determinant in vital outcome; other factors (strategic localization, etc.) might influence long term functional status.
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Five patients were examined suffering from bilateral paramedian thalamic infarction, caused by occlusion of the posterior paramedian thalamo-subthalamic arteries, when they begin from one single pedicle. All cases began with obnubilation or transitory coma, followed by hypersomnia. Four patients showed vertical gaze paralysis, and the fifth vertical nystagmus. In three cases, nuclear lesion of the III cranial nerve was observed along with alteration of the photomotor reflexes, and there was miosis in one case. All were suffering from weakness in one or another limb or facial paresis and generalised acute hypotonia: only one patient had hemihypostesia. All five had dysarthria, ataxy and dysmetria, one had asterixis and two spasmodic crying. Between 5 and 12 months later, one had akinetic mutism and vertical gaze paralysis as the most noteworthy signs. The neuroradiological images show a bilateral ischemic lesion in the paramedian thalamic region, which extends in some cases to the anterior nucleus and in one case to the pulvinars; the lesion continues through the subthalamic regions and the medial part of the mesencephalic tegmentum, with a clear extension to the medial region of the cerebral peduncles in three cases and to the tectum in one case.
We studied the plasma levels and cerebrospinal fluid (CSF) levels in twenty-nine patients suffering from migraine without aura and in eighteen others with aura. The samples were obtained during migraine attacks. We compared the results obtained with those from twenty-seven control subjects. Histidine levels in plasma were 1.18 +/- 0.51 mg/dl for the control group, 1.75 +/- 0.39 mg/dl in those suffering from migraine without aura and 2.07 +/- 0.64 mg/dl in those cases of migraine with aura. In both plasma and in cerebrospinal fluid concentrations of histidine were greater in patients with migraine than in controls (p < 0.001). Histidine is an amino acid precursor of histamine and its abnormalities may be demonstrative of the participation of this amine in migraine attacks, possibly within the state of neuronal hyperexcitability.