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Biomedical subjects

J Castillo

Publications and source records attributed to J Castillo.

At least 109 records · Page 6Linked to original sources

[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↗

[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↗

[The prognostic value of analytical hemorheological factors in stroke].

Plasmatic hyperviscosity is a known vascular risk factor which depends, among other parameters, upon total proteins, haematocrit value and fibrinogen. The aim of this study was to determine the relationship between these analytical haemorrological parameters and mortality and acute stroke sickness rate. We studied 216 patients with brain infarct and spontaneous intracerebral haemorrhage out of a sample of 256 acute stroke patients. We evaluated neurological affectation using the Canadian scale upon admission, on the seventh day and after three months. We determined plasmatic haemorrological factors (haematocrit, fibrinogen and total proteins) upon admission and again after one week and then at three months High fibrinogen levels in plasma were related to brain infarct mortality regardless of the cause of death.

Adult↗

[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↗

[Latent periods in attending patients with acute cerebrovascular disease. A multicenter study].

Treatment of stroke is effective when given straight away at the onset of symptoms. Our objective was to find what the present latent periods in the medical attention of stroke patients are. A study was made in 18 hospital neurology units. The time elapsed between onset of the stroke and being attended by a doctor in the Hospital Emergency Department, by a neurologist and in being admitted to hospital was determined. 794 patients were studied. The average time lapse before attention by the first doctor was 10.7 (0.1-504) hours, in receiving attention in the Emergency Department 14.1 (0.1-505), in being attended by a neurologist 24.3 (0.2-510) hours and in being admitted to hospital 21.3 (0-511) hours. In the first six hours 68.7% of the patients were seen by the first doctor, 58.2% went to the Emergency Department, 22.7% were attended by a neurologist and 22.3% were admitted to a Neurology Unit. The average time between arrival at the Emergency Department and seeing a neurologist was 10.5 (0-67.5) hours. To improve the treatment of stroke, reduction of the latent periods is necessary.

Acute Disease↗

[Perioperative mortality in elderly patients undergoing general surgery].

OBJECTIVE: To determine wether the physical status (ASA category) and surgical conditions could predict mortality in elderly general surgery patients. PATIENTS AND METHODS: This was a prospective study of patients greater than or equal 85 years of age who underwent elective or emergency surgery under general anesthesia between January 1987 and December 1991. Hospital mortality was defined as death occurring before discharge. Logical regression analysis (Cox's modeling) was used to assess group survival. RESULTS: One hundred and nine patients undergoing 117 operations were enrolled. Major surgery was performed in 70%; 44% were removals of malignant tumors and 84% were under general anesthesia. Hospital deaths occurred in 10%; the only significant predictors were neoplastic disease and emergency status. Mortality was 43% one year after surgery; significant predictors of death were prior physical status, neoplasia and emergency status. CONCLUSIONS: Neoplastic disease, emergency status and poor physical condition are factors that predict mortality in patients 85 or older who undergo general surgery.

Aged↗

[Succinylcholine induces hyperpotassemia in patients in critically ill patients].

OBJECTIVE: To study changes in kalemia caused by succinylcholine administration to patients in critical care, and the possible association of succinylcholine with clinical and analytical data, severity-of-disease classification, duration of stay in the intensive care unit (ICU) and immobility. PATIENTS AND METHODS: Twenty-three patients admitted to the ICU, none of whom suffered burns, polytrauma or neuromuscular disease, and who had received 1.5 mg/kg succinylcholine on 28 occasions, usually to facilitate tracheal intubation. Kalemia was analyzed before neuromuscular relaxation and 5 and 30 min afterwards. Electrocardiographic II and V5 derivations and invasive arterial pressure were monitored in all patients. The increase in kalemia at 5 min correlated with age, sex, weight, APACHE II score, days in ICU, current and accumulated immobility, and analytical parameters such as glycemia, creatinine, GOT, bilirubinemia, pH and creatine kinase. The kalemia of these patients was compared with that of 15 patients in acceptable general state who had undergone scheduled surgery. RESULTS: Kalemia increased significantly from a mean baseline level of 4.2 (0.9) mEq/l to 5.5 (1.4) at 5 min and 4.6 (0.9) at 30 min in ICU patients. In the non ICU patients there were no statistically significant changes. Kalemia at 5 min was correlated with baseline (r = 0.84; p < 0.0001), days in the ICU (r = 0.39; p < 0.05) and weight (r = 0.46; p < 0.05). The mean increase in kalemia at 5 min was 0.5 mEq/l in patients who stayed less than 10 days, 1.8 mEq/l in those whose stay was from 10 to 30 days and 1.4 mEq/l in patients who stayed longer than 30 days. The percent increase in kalemia correlated directly (r = 0.7; p < 0.001) with days in the ICU and with accumulated immobility in patients whose ICU stay was less than 30 days. For ICU stays longer than 30 days the correlation was negative (r = -0.98; p = 0.03). Electrocardiographic changes were recorded in 2 patients with brief sinus bradycardia having no hemodynamic repercussions. CONCLUSIONS: The use of succinylcholine in critically ill patients causes a brief but significant increase in kalemia, with slight and rare electrocardiographic changes. The effect varies according to the length of time spent in the ICU and the degree of immobility, with maximum increases seen when the ICU stay is between 10 and 30 days. Patient immobility may play an important pathophysiological role. The indications for use of succinylcholine in critically ill patients should be very strict, particularly during the period of greatest sensitivity.

Adult↗

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↗

Adenosine deaminase activity in the CSF of patients with aseptic meningitis: utility in the diagnosis of tuberculous meningitis or neurobrucellosis.

We assayed 229 CSF samples from 180 adults with meningitis of different etiologies for adenosine deaminase activity (ADA) and evaluated the usefulness of this assay in the differential diagnosis of aseptic meningitis. Cases of meningitis were classified as tuberculous meningitis (TBM), pyogenic meningitis, viral meningitis, self-resolving aseptic meningitis without a specific diagnosis, meningitis associated with other infections, and neoplastic meningitis. We also tested 117 CSF specimens for which parameters were normal. We chose a cutoff point of 10 IU/L on the basis of our results and found elevated ADA levels in 50% of the patients with TBM (no differences between patients with AIDS and those who did not have AIDS were observed). Among samples from patients with aseptic meningitis, we observed high ADA levels in only two of five of the patients with neurobrucellosis. Therefore, we concluded that in cases of aseptic meningitis, a CSF ADA level of > or = 10 IU/L has a sensitivity of 48%, a specificity of 100%, a positive predictive value of 1, and a negative predictive value of 0.91 as a diagnostic criterion for TBM or neurobrucellosis. ADA levels were also > 10 IU/L in 30% of the patients with pyogenic meningitis, but this diagnosis was easily excluded on other grounds.

Adenosine Deaminase↗

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↗

Delay in neurological attention and stroke outcome. Cerebrovascular Diseases Study Group of the Spanish Society of Neurology.

BACKGROUND AND PURPOSE: Despite efforts to reduce the delay between stroke onset and new interventional treatments, no studies have analyzed the repercussions of early neurological attention on the clinical outcome of stroke patients. METHODS: Data were obtained from 721 patients admitted consecutively for a transient ischemic attack or stroke to the neurology departments of 18 Spanish hospitals that followed the same diagnostic and therapeutic guidelines in the acute phase. Factors assessed were age, sex, Canadian Stroke Scale score on admission, previous Barthel Index, and delay before attention by the first physician, by emergency services, by a neurologist, and before hospitalization. Patients' outcomes were classified as good (Barthel Index > 60) or poor (Barthel Index < or = 60 or in-hospital death) depending on patient's functional capacity on discharge. The individual contribution of each of these variables on clinical outcome was estimated with logistic regression analysis. RESULTS: Patients in worse neurological condition on admission presented earlier to the first physician, emergency department, and neurologist. The mortality rate was not significantly modified by early or late presentation at the different medical stages. Logistic regression analysis revealed that the relative risk of poor outcome in patients seen by the neurologist after the first 6 hours from symptom onset was 5.6 (95% confidence interval, 3.4 to 9.2) (P < .0001). Multiple linear regression analysis showed that the delay before the patient received neurological attention correlated positively with the duration of hospitalization (P < .0001). The delays before the patient was seen by the first physician or the emergency department and before hospitalization were not independently related to clinical outcome or length of hospitalization. CONCLUSIONS: Early neurological attention in acute stroke is related to better functional outcome and shorter hospitalization.

Age Factors↗

Failure of talc pleurodesis is associated with increased pleural fibrinolysis.

Diffuse pleural inflammation and fibrin deposition following the instillation of the sclerosing agent is considered necessary for a successful pleural symphysis. We hypothesized that an impairment in fibrin formation or an increased endopleural fibrinolysis would lead to failure of pleurodesis. To investigate changes in the pleural coagulation/fibrinolysis balance, we studied 75 consecutive patients who underwent thoracoscopy. Fifty-four of these patients with malignant pleural effusions and four with a benign recurrent effusion underwent thoracoscopic talc pleurodesis. Another four patients with malignancy and 13 with benign effusions had no talc poudrage performed and were included as a control group. Serial determinations of thrombin-antithrombin III complex (TAT), plasminogen activator inhibitor (PAI), and D-dimer were made in pleural fluid samples taken at the beginning of thoracoscopy (baseline), immediately after thoracoscopic biopsies had been done (postbiopsy), 3 h after thoracoscopy--either with talc poudrage or without--and 24 and 48 h after the procedure, as well as in cases of recurrence of effusions (farline). Successful pleurodesis was obtained in 42 of 52 patients who could be evaluated (81%), and failure was seen in 10. Strong activation of coagulation and production of PAI was observed in all groups, including the control (no talc) group. Fibrinolytic activity (as expressed by D-dimer levels) showed a clear decline 24 h after talc poudrage in patients with a good outcome of pleurodesis, as oppossed to those with bad results and to the control group, and returned to the baseline by 15 d. We conclude that increased pleural fibrinolytic activity is associated with failure of pleurodesis, despite significant inhibitory activity of PAI in all groups.

Antithrombin III↗

Blood dyscrasias with carbamazepine and valproate: a pharmacoepidemiological study of 2,228 patients at risk.

OBJECTIVE: The purpose of this study was to determine the occurrence of leukopenia and other blood dyscrasias associated with psychiatric use of carbamazepine and valproate. METHOD: Rates of WBC counts of 3,000-4,000/mm3 (moderate leukopenia) and < 3,000/mm3 (severe leukopenia), platelet counts of < 100,000/mm3, and hematocrit < 30% were identified among 2,228 treated patients at risk among 11,720 patients admitted to McLean Hospital over 4 years (1989-1993). Patients who received carbamazepine or valproate and had a blood dyscrasia not associated with a relevant medical condition were compared to patients treated with imipramine or desipramine. RESULTS: Of 977 patients treated with carbamazepine, 2.1% experienced leukopenia (16 moderate cases, five severe). Time to 50% risk was 16 days, and recovery occurred within about 6 days after carbamazepine was stopped. For 1,251 patients given valproate, the occurrence of leukopenia was 0.4% (three moderate cases, two severe). The occurrence of leukopenia in 1,031 patients given the tricyclic antidepressants was 0.3% (two moderate cases, one severe). The observed occurrence of moderate leukopenia with carbamazepine was 6.9 and 7.3 times higher than that with valproate and antidepressants, respectively. CONCLUSIONS: Severe blood dyscrasias were uncommon in psychiatric patients given carbamazepine and were about as rare with valproate as with imipramine or desipramine. Most important, in this cohort of 2,228 patients exposed to carbamazepine and valproate, there were no life-threatening cases.

Adolescent↗

[POEMS syndrome. A case report].

A 48 years old male is reported. He presented with lower limb progressive and severe polyneuropathy, hypertrichosis, endocrinological alterations (hypothyroidism and hypogonadism) and organomegaly (hepatosplenomegaly and lymphadenopathies). This syndrome was associated with an osteosclerotic myeloma. The patient died two months after admission.

Hepatomegaly↗