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Biomedical subjects

A Chamorro

Publications and source records attributed to A Chamorro.

At least 55 records · Page 3Linked to original sources
PubMed1997

Periventricular white matter lucencies in patients with lacunar stroke. A marker of too high or too low blood pressure?

BACKGROUND: Periventricular white matter lucencies (PWML) have been described in stroke patients with arterial hypertension, hypotensive episodes, or increased nocturnal fall of blood pressure (BP). As a result of these mixed factors, the relationship between PWML and BP remains unsettled and the appropriate management of arterial BP in stroke patients with PWML is unknown. OBJECTIVE: To clarify the relationship between PWML, arterial BP, and cerebral hemodynamics. DESIGN: Cohort study followed up 6 months after index stroke. SETTING: Referral center. PATIENTS: In 41 consecutive patients with first-ever lacunar infarction, the extent of PWML detected on brain magnetic resonance images was measured. Six months after stroke, BP values were monitored during a 24-hour period and transcranial Doppler examinations were performed at rest and following the administration of acetazolamide. MAIN OUTCOME MEASURES: Correlation of cerebral hemodynamics and BP values with the extent of PWML. RESULTS: The severity of PWML varied substantially among patients, suggesting that PWML and lacunar infarctions could be due to several different mechanisms. Older age, elevated awake systolic BP, increased cerebrovascular tone, and the interaction between history of heart disease and the lowest heart rate were the strongest independent predictors of the severity of PWML. Diastolic BP and the vasodilatory capacity of the resistance vessels did not predict the severity of PWML. CONCLUSIONS: Overall, PWML are markers of systolic damage in older lacunar stroke patients with stiffer arteries. In addition, hemodynamic failure may be relevant in patients with concomitant heart disease.

Aged↗
PubMed1997

Blink reflex in patients with Wallenberg's syndrome.

Knowledge of the neural circuits involved in Wallenberg's syndrome (WS) is incomplete. Study of the blink reflex (BR) in patients with WS can help in reaching a better understanding of the physiopathology underlying clinical symptoms and may help in the prediction of clinical outcome. We evaluated the BR in response to supraorbital nerve electrical stimuli in 20 patients with WS. All patients were studied within the 1st week after onset of symptoms, and 10 of them were also studied repeatedly during a follow-up period of 3-12 months. At the first examination the long latency bilateral responses (R2 and R2c) to stimulation of the supraorbital nerve of the affected side were absent in 11, delayed in 4, and normal in 5 patients. At follow-up, there was a normalization of the BR in all patients who had absent or delayed responses at the first examination except for one patient whose responses remained absent at the 9th month. Late responses elicited on the side of the lesion by stimulation of the non-affected supraorbital nerve were normal in all but one patient. This patient died from cardiorespiratory arrest within the 1st month of the illness. One patient with normal BR responses also died in the acute phase. The BR is abnormal in most patients with acute WS and tends to normalize in a mean period of 7 months. BR pattern is not a predictor of early fatal complications in patients with this syndrome.

Adult↗
PubMed1997

Ballistic movements due to ischemic infarcts after intravenous heroin overdose: report of two cases.

Stroke is an infrequent but recognized complication of heroin addiction. Two heroin addicts, aged 34 and 19 years, developed ballistic movements after intravenous heroin overdose. Patient 1 presented bilateral ballism 1 week after intravenous heroin injection. Magnetic resonance imaging (MRI) showed bilateral ischemic lesions of the globus pallidus, suggesting a generalized cerebral hypoxia during the comatose state as pathogenic mechanism. Patient 2 presented an acute left hemiballismus when consciousness was restored with naloxone. MRI demonstrated an ischemic infarct in the right striatum. An embolic mechanism of stroke was suspected in this patient, considering the normal results of blood analysis, echocardiogram and cerebral arteriograms. Ballistic movements ceased after administration of haloperidol; both patients remained without abnormal movements thereafter.

Adult↗
PubMed1997

Chorea in the antiphospholipid syndrome. Clinical, radiologic, and immunologic characteristics of 50 patients from our clinics and the recent literature.

We analyzed the clinical, radiologic, and immunologic characteristics of 50 patients with chorea and the antiphospholipid syndrome (APS) (6 from our clinics and 44 from a MEDLINE computer-assisted review of the literature from 1985 through 1995). Forty-eight (96%) patients were female and 2 (4%) were male. Twenty-nine (58%) patients had defined systemic lupus erythematosus (SLE), 6 (12%) had "lupus-like" syndrome, and 15 (30%) patients had "primary" APS. Mean age of patients in this series was 23 +/- 12 years (range, 6-77 yr); mean age at presentation of chorea was 21 +/- 12 years (range, 6-77 yr). In 11 (22%) patients, the onset of chorea was in childhood (6-14 yr), and in 2 (4%) patients it presented at 60 years or more. Six (12%) patients developed chorea soon after they started taking estrogen-containing oral contraceptives, 3 (6%) developed chorea gravidarum, and 1 (2%) patient developed chorea shortly after delivery. Most patients (66%) presented only 1 episode of chorea. Chorea was bilateral in 55% of patients. Computed tomography and magnetic resonance imaging scans reported cerebral infarcts in 35% of patients. The following antibodies were detected: lupus anticoagulant (92%), anticardiolipin antibodies (91%), antinuclear antibodies (82%), anti-DNA (59%), anti-Ro (10%), anti-RNP (8%), anti-La (2%), and anti-Sm (2%). The chorea in these patients responded to a variety of medications, for example, steroids, haloperidol, antiaggregants, anticoagulants, or a combination of therapy, usually prescribed in the presence of other manifestations of APS or SLE. However, many patients responded well to haloperidol and to the discontinuation of oral contraceptives if this was the precipitating factor.

Adolescent↗
PubMed1997

Motor behavior in stroke patients with isolated medial frontal ischemic infarction.

BACKGROUND AND PURPOSE: Current interpretation of hemiparesis in anterior cerebral artery infarction holds that whereas leg weakness correlates with destruction of the corticospinal tract at the paracentral lobe, faciobrachial symptoms indicate extension of the infarct to the upper lateral convexity or to subcortical structures, where the corticospinal tract subserving the arm would be interrupted. We analyzed the motor behavior in eight patients with purely medial hemispheric infarctions who had face, arm, and leg involvement. METHODS: In addition to careful clinical testing, we performed neuroimaging or pathological studies to exclude the involvement of the primary motor cortex or subcortical structures. Motor function was further tested in three patients by studying the reaction time to an auditory stimulus and by stimulating the motor cortex and the cervical and lumbar spine with a magnetic stimulator. RESULTS: All patients had signs of motor neglect, such as lack of spontaneous movement in the upper limb, unilateral reaction to pain stimuli, clumsy voluntary movements, or motor impairment on bimanual tasks. Electrophysiologically, we found absent or poor voluntary activity in both upper and lower limbs contralateral to the infarction. However, whereas cortical stimulation showed absent responses in the lower limb, it disclosed normal latencies in the upper limb, indicating that the corticospinal tract to paretic muscles of the upper limb was intact. CONCLUSIONS: Our findings suggest that faciobrachial symptoms in purely medial hemispheric infarctions in the anterior cerebral artery territory reflect motor neglect caused not by involvement of primary motor pathways but by damage to medial premotor areas.

Aged↗
PubMed1997

[The effect of clinical trials on hospital admission for stroke].

OBJECTIVE: To analyze the contribution of clinical trials in the hospital treatment of acute ischaemic cerebrovascular disease. DEVELOPMENT: In recent studies many trials have been designed for the treatment of the acute phase of this illness. Based on experimental studies, the drugs used in the trial need to be given within a 'therapeutic window' of less than six hours from the onset of the illness. This time factor has led to a radical change in the organization of hospital services dealing with this illness. In order to run clinical trials the medical staff have had to be organized into functional stroke units for the swift protocolized diagnosis of the condition. Also information has to be given to health workers regarding the need for urgent specialized treatment. Several studies have shown that early, specialist treatment reduces morbi-mortality, time spent in hospital and financial cost in these patients. CONCLUSION: Clinical trials in acute cerebrovascular pathology have formed the basis for the creation of stroke units, led to the drawing up of protocols for the diagnosis and guidelines for treatment. It has also made the medical profession more aware of the importance of early diagnosis and specialized treatment in acute cerebral ischaemia.

Brain Ischemia↗
PubMed1996

Brain stem reflexes in patients with Wallenberg's syndrome: correlation with clinical and magnetic resonance imaging (MRI) findings.

In spite of the general clinical uniformity of Wallenberg's syndrome (WS), individual patients present with a slightly different clinical picture, and detailed studies with magnetic resonance imaging (MRI) show differences in the topography of the brain stem lesion. Neurophysiological characterization of the lesion in WS has been known for a long time, but there are no studies on the possible correlation between lesion topography and neurophysiological deficit. Assuming that afferents from the three branches of the trigeminal nerve reach different parts of the trigeminal nuclei, we examined the possible correlation between the lesion topography assessed by the MRI and the neurophysiological deficit, assessed by studying the brain stem reflexes in patients with WS within 2 weeks after stroke. Neurophysiological abnormalities were always located in the afferent branch of the reflexes examined, but not all patients exhibited abnormalities in all responses. The ophthalmic branch was involved in 92.8% of patients, and the mandibular branch in 57.1% of patients. The patients with MRI lesions located in the lower medulla had normal responses with infraorbital or mental nerve stimulation. The results of this neurophysiological study confirm the heterogeneity of WS. Whether the neurophysiological identification of different subgoups of patients is relevant for clinical outcome needs further studies.

Action Potentials↗
PubMed1996

Contribution of arterial blood pressure to the clinical expression of lacunar infarction.

BACKGROUND AND PURPOSE: The relation between symptomatic lacunar infarction, silent stroke, and arterial hypertension is controversial. METHODS: From 500 patients with ischemic or hemorrhagic stroke admitted to the Downtown Barcelona Stroke Registry between July 1992 and December 1994, we evaluated prospectively the prevalence of silent infarction in 249 patients who had a brain MRI. The association of risk factors with silent infarction was investigated with the use of logistic regression analysis. In a selected group of 43 patients with symptomatic lacunes, we performed at stroke follow-up transcranial Doppler sonography and 24-hour continuous blood pressure monitoring to evaluate whether blood pressure, cerebrovascular tone, and cerebral blood flow at rest and after the administration of 1 g acetazolamide correlated with silent infarction. RESULTS: A total of 147 silent infarctions were observed in 83 patients (33%). Most silent infarctions corresponded to small deep lesions in the territory of the lenticulostriate arteries. Patients with silent infarctions had higher systolic and diastolic blood pressure at stroke onset. However, on multivariate analysis, age greater than 60 years was the only risk factor associated with silent infarction. In a subgroup of 43 patients with symptomatic lacunes and patent extracranial vessels, systolic and diastolic pressure at stroke onset and diastolic pressure and vascular resistance at stroke follow-up were higher when silent infarctions co-existed. However, cerebral blood flow at rest and after acetazolamide injection were unrelated to silent infarction. CONCLUSIONS: Silent ischemia in patients with symptomatic lacunar and nonlacunar stroke was only associated with aging. However, a history of arterial hypertension was perhaps unrecognized, since hemodynamic testing and continuous blood pressure monitoring in patients with lacunar stroke suggested that the coexistence of silent lesions indicated a more generalized cerebral arteriolosclerosis.

Acetazolamide↗
PubMed1995

Liver transplantation in patients with Budd-Chiari syndrome.

Patients with Budd-Chiari syndrome (obstruction of the hepatic veins) and associated hepatic insufficiency may be candidates for orthotopic liver transplantation (OLT). In our series of 405 OLT patients, 3 were transplanted due to Budd-Chiari syndrome (0.7%). The indication for liver transplantation in these patients was severe hepatic insufficiency (chronic in two and acute in the third one). Morphologic study of the obstructions revealed apparently different causes, including thrombi, membranous webs in hepatic veins, and hydatid cyst compression. The surgical technique employed in these transplantations was similar to that for other etiologies. Due to its implications for the future course of OLT, it is important to determine the exact etiology of Budd-Chiari syndrome in the pretransplant period and to treat the patients with early and long-term anticoagulant therapy to avoid syndrome recurrence.

Adolescent↗
PubMed1995

Early prediction of stroke severity. Role of the erythrocyte sedimentation rate.

BACKGROUND AND PURPOSE: Early predictors of functional outcome after stroke are necessary for better planning of treatment and care. METHODS: We evaluated prospectively early clinical predictors of short-term functional outcome in a group of patients with ischemic cerebral infarction and explored whether the intensity of the acute-phase response provided further information concerning the short-term functional outcome. We evaluated a group of 208 ischemic stroke patients using the Mathew scale at entry. All patients had neuroimaging studies and routine blood tests, including erythrocyte sedimentation rate (ESR), within 72 hours from clinical onset. At discharge, functional outcome was graded according to a Stroke Outcome Scale. RESULTS: Larger infarcts, more embolic infarcts, and fewer lacunar infarcts were observed in the poor-outcome group. Vascular risk factors, radiological findings not related to the index stroke, time to admission, and treatment were similar in the two outcome groups. Variables with statistically significant differences between outcome groups included the following: age > 65 years, female sex, admission Mathew score < 75, worsening at clinical presentation, infarct volume > 6 cm3, complicating infections, fasting glucose > 110 mg, nonfasting glucose > 130 mg, and elevated ESR. With stepwise logistic regression analysis, Mathew score on admission, infarct volume, mode of clinical presentation, and ESR remained in the predictive model of stroke outcome, with a sensitivity and specificity of 89.91% and 85.71%, respectively. After removing the computed tomographic information from the model the same variables remained, with a sensitivity and specificity of 83.05% and 94.29%, respectively. CONCLUSIONS: Infarct size and clinical severity on admission are the stronger predictors of short-term functional outcome. Mode of clinical presentation, clinical evolution during the first day of stroke, and ESR are also independent predictors of short-term stroke outcome. These findings might be indicative of an inadequate collateral profile and/or a more pronounced prothrombotic state.

Adult↗
PubMed1995

Early anticoagulation after large cerebral embolic infarction: a safety study.

OBJECTIVE: To assess whether hemorrhage after early anticoagulation in nonseptic embolic infarction is related to clinical severity and infarction size. BACKGROUND: Explicit clinical criteria and timing of anticoagulation after large embolic infarctions are unknown. METHODS: Out of 171 patients receiving anticoagulation between July 1992 and December 1993, 83 patients with hemispheric embolisms received heparin within 72 hours from onset (activated partial thromboplastin time [aPTT] 1.5 times control value). Stratified by age and sex, a "high-risk" group (46 patients) was defined as those having stroke symptoms involving three or more CNS domains, Mathew Scale score < or = 74, or hemorrhagic infarction on initial CT, and a "low-risk" group (37 patients) as those having stroke symptoms involving fewer than three cortical domains, or Mathew Scale score > 74, and CT showing no blood. Loss of consciousness, seizures, or history of bleeding were exclusion criteria. Repeated CTs (100%) and MRIs (36%) detailed infarctions according to standard maps and evaluated all unexplained clinical worsening. RESULTS: Prior to therapy, high-risk patients had more severe clinical deficits (p < 0.01), larger infarctions on CT (p < 0.01), and more mass effect (p < 0.01). Hemorrhagic conversion (26% in the high-risk group versus 22% in the low-risk group) and hemorrhagic worsening (4% in the high-risk group versus 13% in the low-risk group) were unrelated to admission clinical severity or infarction size, but they were related to an excessive prolongation of the aPTT (p < 0.01). CONCLUSIONS: Infarction size and clinical severity in alert patients with nonseptic embolic stroke carries no additional bleeding complications after early anticoagulation. If anticoagulants are deemed necessary, treatment delay seems unjustified. However, rigorous monitoring of the aPTT is strongly advised to keep the level at 1.5 to 2 times control values.

Aged↗
PubMed1995

[Critical analysis of early heparin therapy in cerebral ischemic infarction].

This is a critical review of the role of heparin in the acute phase of ischemic cerebral vascular accident (CVA). Completed clinical trials lead to the following conclusions: 1. The efficacy of heparin in the acute phase of CVA is unknown, given the many biases and methodological imprecisions contained in the studies performed so far, among them a reliance on temporal rather than etiological classification of infarctions and the small number of patients treated. 2. Heparin-related complications have been explored only anecdotally and retrospectively, even though the risk of hemorrhage would depend on the magnitude of the prolongation of PTTa. The severity of neurological deficit, infarction size and patient age, on the other hand, would be contributing factors. 3. Delay in start of heparin therapy based on the severity of clinical symptoms is not supported by the evidence. There are prospective studies, on the other hand, that indicate a lack of correlation between early instauration of heparin therapy and the appearance of complications in severe stroke. 4. PTTa must be controlled carefully in the heparinized patient and administration of the drug in continuous perfusion or by subcutaneous injection is recommended.

Brain↗