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Biomedical subjects

J L Martí-Vilalta

Publications and source records attributed to J L Martí-Vilalta.

At least 19 recordsLinked to original sources

Diagnostic yield of prothrombotic state studies in cryptogenic stroke.

OBJECTIVES: Around 30% of ischemic strokes are considered cryptogenic. We analyzed the diagnostic yield of prothrombotic state (PS) studies in patients with an initial cryptogenic stroke (CS). MATERIAL AND METHODS: We prospectively included consecutive CS patients according to the TOAST criteria. PS included plasmatic determinations of antiphospholipid (APL) antibodies and lupus anticoagulant (LA), S (SPd) and C (CPd) protein deficiencies, and genetic analysis of the prothrombin gene mutation (PT G20210A) and the factor V Leiden mutation (FV G1691A). We recorded age, sex and vascular risk factors. RESULTS: From a total of 89 patients (mean age 56.9 +/- 14.3 years, 53% men), we identified 16 PS in 15 patients (16.85%): APL-6, LA-2, SPd-2, CPd-1, PT G20210A -3 and FV G1691A -2. One patient presented an association (APL and PT G20210A). CONCLUSIONS: One of every six patients with initial CS present a PS. Age or sex and conventional cardiovascular risk factors were not related to PS study findings, supporting the relevance of such studies in all patients with an initial CS.

Adult↗

Stroke and pulmonary thromboembolism after a long flight.

In the economy class syndrome (ECS) the patient presents a deep venous thrombosis (DVT) with or without pulmonary thromboembolism (PTE) during or after a long trip as a result of prolonged immobilization. Economy class stroke syndrome is an infrequent ECS variant in which ischemic stroke is associated with a patent foramen ovale (PFO). Few cases have been published in the literature to date. We present a patient who suffered a PTE and an ischemic stroke immediately after a transoceanic flight. A 36-year-old woman with no significant medical or familial history flew economy class from Lima, Peru, to Madrid, Spain. On disembarkation she presented sudden dyspnea and a depressed level of consciousness, global aphasia, and right hemiparesis. A pulmonary scintigraphy showed a PTE and a cranial MRI revealed an ischemic infarct in the left middle cerebral artery territory. We simultaneously performed a transesophageal echocardiography and a transcranial Doppler and observed a massive right-to-left shunt through a PFO. The patient was a heterozygous carrier of the C46T mutation of coagulation factor XII. The appearance of a stroke following a long trip is suggestive of paradoxical embolism through a PFO, mainly if it is associated with a DVT and/or a PTE. The cause of the initial event, the DVT, could be a prothrombotic state.

Adult↗

[Percutaneous transluminal angioplasty of the subclavian artery in Takayasu disease: results of long-term follow-up].

Takayasu arteritis is a chronic inflammatory arteriopathy of unknown etiology affecting the aorta and proximal portion of its main branches. Although it was initially reported in young women of Oriental descent, its current worldwide distribution is known to affect both sexes. In the last decade, percutaneous transluminal angioplasty (PTA) has emerged as a viable alternative in its treatment. However, the percentage of restenosis is more common in Takayasu disease than atherosclerotic lesions (21% vs 10%), probably due to diffuse inflammatory vascular involvement. Since the introduction of stent, this technique has emerged as a viable alternative to treatment of atherosclerotic stenotic lesions, although its efficacy and safety in Takayasu disease is still unclear. Herein, we report our experience in a woman with subclavian steal syndrome in whom Takayasu disease was diagnosed and treated with subclavian artery angioplasty and stent, with a good outcome during four years of follow-up.

Adult↗

New concepts in lacunar stroke etiology: the constellation of small-vessel arterial disease.

OBJECTIVE: To update the less frequent etiologies causing lacunar infarcts (LIs). To highlight recent advances in risk factors, clinical syndromes, topography, complementary tests and long-term prognosis in this subtype of ischemic stroke. PATIENTS AND METHODS: The most important studies are analyzed, from CM Fisher works, selecting those referring to LIs of unusual etiology, and recent advances and controversies in the clinical management of LI are discussed. RESULTS: LIs are found in approximately 11% of patients admitted with stroke. The pure motor hemiparesis (55%) constitutes the most usual lacunar syndrome. However, lacunar syndromes may not be caused by LIs in 10-20% of cases. LIs caused by microembolism and cholesterol embolism from the aortic arch are reviewed. Hematological diseases can also cause LI, such as polycythemia rubra vera, essential thrombocythemia and primary antiphospholipidic antibody syndrome. Other etiologies are carotid plaque embolism, severe stenosis of a perforated arteriole and amyloid angiopathy. Infectious arteritis by neurolues, neurocysticercosis, neuroborreliosis, by AIDS or Helicobacter pylori infection have also been associated with the presence of LIs. Likewise, inflammatory arteritis in systemic lupus erythematosus or granulomatous angiitis, cocaine abuse and panarteritis nodosa have been related to LI, although in the latter LI would be caused by a thrombotic microangiopathy and not by vasculitis. CONCLUSIONS: LI is an ischemic stroke subtype with a characteristic clinical presentation and a short-term favorable prognosis. Although high blood pressure constitutes the main risk factor and the main etiology, LIs may be caused, in less than 5% of cases, by various etiologies, mainly hematological diseases and infectious or inflammatory arteritis. It is essential to make a correct etiological diagnosis for LI as treatment will be different according to its etiology.

Arteritis↗

[Intracerebral haemorrhage by cerebral hyperperfusion after carotid angioplasty in a tandem lesion. A case report].

Intracerebral hemorrhage (ICH) by hyperperfusion after carotid angioplasty has a frequency of 1.2 % - 4.4% in the literature. Until now no case of ICH after carotid angioplasty in a tandem lesion has been reported. We present the case of a patient who suffered an ICH due to the hyperperfusion syndrome, after carotid angioplasty of two stenotic lesions of the left internal carotid artery (ICA) (intracranial and extracranial). He was a 58 year old man who suffered repetitive left carotid TIA despite being treated with antiplatelet therapy. An angiogram showed 76 % extracranial stenosis and 96 % intracranial stenosis of the left ICA as well as 59 % extracranial stenosis of right ICA. Angioplasty with stenting of the two stenosis of the left ICA was performed. After 48 hours of the angioplasty, the patient presented a massive ICH and died a few hours later. ICH by hyperperfusion is an infrequent complication of the carotid angioplasty. The risk factors of the ICH should be evaluated in order to decrease their incidence as well as to maintain an intensive control of the arterial pressure during and after the procedure. This case is the first one published after angioplasty of a tandem lesion. It is possible that the pathophysiologic mechanism involved was an excessively rapid restitution of the normal arterial size.

Angioplasty↗

[Leukoaraiosis. Clinical importance and prognosis].

Advance in the health care systems, in medical knowledge and improvements in quality of life have contributed to the fact that life expectancy of the persons in developed countries exceeds 80 years of age. This has made it possible to observe the increase in frequency of common diseases of the elderly, one of the most relevant of which is dementia. The two most frequent etiologies of dementia are the degenerative one, with Alzheimer's disease (AD) as the main cause, and those of vascular etiology or vascular dementia, within which subcortical arteriosclerotic encephalopaty or Binswanger's disease (BD) are found with low prevalence. Since, on one hand, diagnosis of the dementias is not enough or definitive by clinical means, and on the other hand, the pathological diagnosis does not modify the evolution of disease, emphasis is presently placed on diagnosis by neuroimaging studies. In recent years, with the coming of the computerized tomography (CT) and the magnetic resonance (MR), it has been possible to observe lesions in the white matter of the brain hemisphere in patients with these two etiologic groups of dementias, that is, degenerative and vascular, as well as in elderly patient without cognitive deterioration, with or without vascular risk factors.

Alzheimer Disease↗

[Asystolias in the acute phase of brain stroke. Report of a case].

Brain areas involved in heart autonomic control are not well characterized. Insulae have been proposed as control centers. A lesion in these areas may induce a cardiac autonomic dysfunction (arrhythmias, atrioventricular conduction abnormalities). Asystolia has not been previously reported. A 65-year-old man suffered an acute ischemia of the right middle cerebral artery (MCA) territory. NIHSS score was 19 points. Brain CT scan was normal. Transcranial Doppler (TCD) showed occlusion of the right MCA. Fibrinolysis was initiated 135 minutes after stroke onset with TCD monitoring. Twenty minutes later he suffered cardiac arrest with asystolia trace in the ECG monitor. Fibrinolysis was stopped during resuscitation. Four minutes later, he recovered with the same NIHSS score. Aggressive resuscitation maneuvers were not necessary. A repeated brain CT scan showed infarct signs in the whole MCA territory and a new TCD did not show any change. Serial blood analyses including cardiac nzymes were normal. The patient experienced four brief cardiac arrests in the next nine hours, so a temporary cardiac pacemaker was placed for four days. He was treated with aspirin and was discharged 14 days after admission. He has not experienced recurrences during a 6-month follow-up. We could not diagnose the etiology of the cardiac arrests. All the episodes occurred in the acute stroke stage and arrhythmia, atrioventricular block, myocardial ischemia or structural lesions were not found in the cardiac study. We propose that ischemia in the right insula induced sudden and transitory interruptions of the sympathetic cardiac tone.

Aged↗

Cerebral perfusion and haemodynamics measured by SPET in symptom-free patients with transient ischaemic attack: clinical implications.

Transient ischaemic attacks (TIAs) are heterogeneous from the clinical, physiopathological, aetiological and prognostic points of view. Single-photon emission tomography (SPET) may influence patient management by helping to define the vascular topography and by suggesting the probable mechanism (embolic or haemodynamic). However, the variables predicting focal regional cerebral blood flow (rCBF) and cerebrovascular reserve (CVR) abnormalities on SPET and their clinical correlation are poorly known. Our objective in this study was to assess the value of rCBF and CVR measured by SPET in a prospective series of 42 patients with recent (within the preceding 30 days) first-ever TIA Two SPET examinations [baseline and post-acetazolamide (ACZ)] were consecutively performed, and region/reference ratios were obtained using an irregular region of interest (ROI) method. Percentages of interhemispheric asymmetry between homologous brain regions were used to identify abnormalities on baseline SPET, and the percentage changes in asymmetry between the baseline and post-ACZ SPET studies were used to identify abnormal responses to the vasodilator stimulus. Mean baseline and test-retest values previously obtained in normals were used as a reference. The relationship of SPET findings with clinical data and results of complementary examinations was assessed. Most patients (98%) had abnormal findings on either baseline (43%), post-ACZ (19%) or both SPET studies (36%). Thus, 33 patients had hypoperfusion on baseline SPET (78.5%, symptom related in 45%). In 23 patients, a poor response to ACZ was found (55%, symptom related in 21.5%). No predictors for rCBF or CVR impairment were found. Most patients with a first-ever TIA episode present focal hypoperfusion on SPET, either with or without correlation with TIA symptoms. Post-ACZ SPET increases the probability of finding cerebrovascular abnormalities, and orients attention towards an haemodynamic compromise. Focal hypoperfusion on SPET should not be viewed as clinically insignificant because it probably reflects previous or ongoing clinical and/or subclinical episodes of cerebral ischaemia.

Acetazolamide↗

The effect of medial frontal and posterior parietal demyelinating lesions on stroop interference.

Functional imaging has consistently shown that attention-related areas of medial frontal and posterior parietal cortices are active during the attentional conflict induced by color naming in the presence of distracting words (Stroop task). Such studies, however, have provided few details of the correlational nature between observed regional brain activations and reaction time delay occurring in this situation. We analyzed the effect of medial frontal and posterior parietal lesions on the Stroop response in a group of patients with multiple sclerosis, a neurological disorder in which Stroop response speed is affected to varying degrees. Forty-five patients were assessed using a computer-presented verbal version of the Stroop task and specific MRI protocol. Demyelination areas were measured on five anatomical divisions of the medial frontal white matter and on white matter of the posterior parietal lobe. We found that a combination of frontal and parietal lesion measurements accounted for 45% of the Stroop interference time variance. Patients with more right frontal than left parietal demyelination showed slowed Stroop responses, whereas the predominance of lesions in the left posterior parietal region was associated with a reduced Stroop interference. These results may contribute to defining the specific participation of these attention-related brain areas in the conflict of attention represented by the Stroop paradigm. They also help to explain the variability of the Stroop effect in multiple sclerosis patients and suggest that the Stroop test does not assess just a single cognitive operation, but rather the combined effect of anatomically segregated neural processes.

Adult↗

Blood pressure variability and leukoaraiosis amount in cerebral small-vessel disease.

OBJECTIVES: To analyze the correlation between blood pressure (BP) variability and leukoaraiosis (LA) amount in patients with symptomatic cerebral small-vessel disease. MATERIALS AND METHODS: We included 25 hypertensive patients: 13 with Binswanger's disease (BD) and 12 with a first-ever lacunar infarction (LI). Baseline office BP was obtained for 3 consecutive weeks. From a 24-h ambulatory BP monitoring performed 1 week later we obtained average systolic (SBP) and diastolic (DBP) BP for daytime, nighttime and 24-h periods. SBP and DBP variability was defined as the within-subject standard deviation of all readings. A standardized cerebral MR was performed in each patient and an LA score was calculated. RESULTS: No statistically significant correlation was obtained between the LA score and any of the following BP values: 1) Baseline SBP and DBP; 2) 24-h, daytime or nighttime SBP and DBP, and 3) 24-h, daytime or nighttime SBP and DBP variability. CONCLUSION: Increased BP variability is not associated with greater amounts of leukoaraiosis.

Aged↗

Blood pressure variability in Binswanger's disease and isolated lacunar infarction.

UNLABELLED: To determine whether blood pressure (BP) variability is increased in hypertensive patients with Binswanger's disease (BD), we studied two samples of consecutive treated hypertensive patients: (1) 11 with BD (mean age 71.3 +/- 5.2 years); (2) 16 with lacunar infarction (mean age 65.2 +/- 8.3 years) without cognitive impairment. An averaged baseline office BP was obtained for 3 consecutive weeks. Ambulatory BP monitoring was then carried out to obtain the averaged mean systolic (SBP) and diastolic BP, and BP variability was defined as the standard deviation of consecutive BP values. RESULTS: Diurnal SBP variability was significantly increased in the BD group (p = 0.04). However, with the analysis of covariance for age and baseline office BP, the difference was no longer significant (p = 0.17 and p = 0.09, respectively). We conclude that increased BP variability in BD patients is probably due to older age and increased baseline office BP. Increased BP variability may be a risk factor for small-vessel disease, but not for cognitive impairment.

Age Factors↗

Beck Depression Inventory factors related to demyelinating lesions of the left arcuate fasciculus region.

This study was conducted to further establish the significance of the previously reported association between depressive symptoms and demyelinating lesions in the region of the left arcuate fasciculus in multiple sclerosis patients. The Beck Depression Inventory (BDI) was broken down into its main symptom categories on the basis of well-established factor analyses from the literature, and the correlation pattern between the resulting BDI subscores and lesion measurements was analyzed. We found that lesions of the left arcuate fasciculus region were selectively associated with BDI items expressing patients' Affective Symptoms and Somatic Complaints. Specifically, lesion measurements from this brain location accounted for 26% of symptom score variance of the BDI part that includes only these two factors. Performance Difficulties and Cognitive Distortions were not consistently associated with the lesion measurement. Performance Difficulties, however, showed a high correlation with the neurologic deficit detected in the physical examination. These results show that lesions in the left arcuate fasciculus region are associated with the core of the depressive syndrome rather than marginal symptoms and, thus, further suggest that this left suprainsular brain region involves white matter tracts relevant to mood regulation.

Adult↗

[Hospital mortality in subarachnoid hemorrhage. Experience of the "Barcelona Registry of Cerebrovascular Diseases"].

OBJECTIVES: To determine clinical predictors of in-hospital mortality in patients with non-traumatic subarachnoid hemorrhage. PATIENTS AND METHODS: Data de 184 patients with subarachnoid hemorrhage were obtained from consecutive stroke included in the prospective "Barcelona Stroke Registry". Demographic, anamnestic, clinical, neuroimaging and outcome variables in the subgroup of patients who died were compared with those in the surviving subgroup. The independent predictive value of each variable on the development of death was assessed with a logistic regression analysis. Three predictive models were constructed. A first model was based on demographic and clinical variables (total 10 variables). A second model was based on demographic, clinical and neuroimaging variables (total 17). A third model was based on demographic, clinical, neuroimaging and outcome variables (total 21). RESULTS: In-hospital death was observed in 44 patients (24%). Transient neurological deficit (OR = 13.92; 95% CI: 1.01-191.95), progressive deficit (OR = 4.21; 95% IC: 1.28-13.86), limb weakness (OR = 3.24; 95% IC: 1.49-7.08) and age (OR = 1.05; 95% CI: 1.02-1.09) appeared to be independent prognostic factors of in-hospital mortality in the first predictive model. In addition to these variables, intraventricular hemorrhage (OR = 5.51; 95% CI: 1.94-16.04) was selected in the second predictive model. Transient neurological deficit (OR = 41.2; 95% CI: 1.61-1056.2), neurological complications (OR = 11.04; CI del 95%: 3.85-31.74), carotid aneurysm (OR = 6.61; 95% CI: 1.23-35.43), intraventricular hemorrhage (OR = 5.51; 95% CI: 1.65-18.4), progressive deficit (OR = 5.35; 95% CI: 1.11-25.90) and hemispheric intracerebral hemorrhage (OR = 4.32; 95% CI: 1.35-13.90), appeared to be independent prognostic factors of in-hospital mortality in the third model. CONCLUSIONS: Clinical features easily obtained at the patient's bedside in addition to neuroimaging data easily obtained in routine neuroimaging studies help clinicians to predict in-hospital mortality in patients with subarachnoid hemorrhage. Transient neurological deficit prior to definitive subarachnoid hemorrhage was the main clinical predictor of in-hospital mortality.

Aged↗

[Cerebral venous thrombosis. Study of 17 cases].

BACKGROUND: We undertook this study to determine the clinical, neuroimaging findings, etiologies and final outcome of 17 patients with cerebral venous thrombosis diagnosed in a single center. PATIENTS AND METHODS: In this retrospective study we analyzed the clinical and neuroimaging findings of patients with cerebral venous thrombosis collected at our hospital from 1980 to 1997. The diagnosis of cerebral venous thrombosis was made by angiography and/or magnetic resonance imaging. Final outcome was assessed with the modified Rankin scale and patients were included in two groups. Differences between groups were tested using uni and multivariate analysis. RESULTS: Seventeen patients (10 women) with a mean age of 41.9 years were analyzed. The most frequent clinical pattern was focal cerebral signs (70.5%) followed by symptoms/signs of increased intracranial pressure (12%) and diffuse encephalopathy (12%). The diagnosis of cerebral venous thrombosis was made by conventional angiography in 12 cases (70.5%) and by magnetic resonance imaging in 5 (29.5%). The most frequent site of venous occlusion was superior sagittal sinus (47%) followed by lateral sinus (35%). Etiologies were hematologic disease (29%), neoplasms (23.5%), oral contraceptives (12%), infection (12%) and unknown in 18%. The majority of the patients (59%) had minor neurological sequelae during follow-up. A decreased level of consciousness and neoplasm were associated with a worse functional outcome. CONCLUSIONS: In our series the most frequent clinical pattern was focal cerebral signs and the main etiology was hematologic disease. A relatively good prognosis was observed in those patients. A decreased level of consciousness and presence of neoplasm were the factors associated with a bad prognosis in these cases.

Adult↗

Spontaneous primary intraventricular hemorrhage: clinical data, etiology and outcome.

The clinical features, etiology, and neurological outcome in patients with primary intraventricular hemorrhage (PIVH) have rarely been reported. We retrospectively reviewed the clinical data, complementary examinations, outcome, computed tomography (CT) blood amount, and ventricle size of 13 patients (mean age 60 years, five men). We defined PIVH as hemorrhage detected by CT in the ventricular system only. The major symptoms included headache (n = 13), decreased level of consciousness (n = 9), and nausea/vomiting (n = 7). The cause was unknown in five patients; and was associated with arterial hypertension in five, vascular malformations in two, and tumor in one, although arteriography was performed in only five patients. Outcomes were death in three, asymptomatic in six, mild disability in three, and moderate disability in one. Prognosis was not related to clinical or CT data. Clinical features can suggest the diagnosis of PIVH, but cerebral CT is required for confirmation.

Adolescent↗

Predictive clinical factors of very early in-hospital mortality in subarachnoid hemorrhage.

This study was conducted to determine clinical predictors of very early in-hospital mortality (within the first 72 h) in patients with non-traumatic subarachnoid hemorrhage. Data of 184 patients with subarachnoid hemorrhage were obtained from consecutive stroke patients included in the prospective Barcelona Stroke Registry. Demographic, anamnestic, clinical, neurological and neuroimaging variables in the subgroup of patients who died within 72 h after the onset of symptoms were compared with those in the subgroup of patients that had survived this initial period. The independent predictive value of each variable on the development of very early death was assessed with a logistic regression analysis. Very early in-hospital death was observed in 18 patients (9.8%). These patients were significantly more likely to have progressive deficit, seizures, altered consciousness, limb weakness, sensory involvement and basal ganglia hematoma than patients without very early death. After multivariate analysis, only progressive deficit (odds ratio (OR) 6.90; 95% confidence interval (95% CI) 2-23.80) and limb weakness (OR 5.46; 95% CI 1.78-16.77) were independent clinical predictors of very early mortality. Progressive neurological deficit and limb weakness at the onset of stroke was independent predictive factors of very early death in patients with non-traumatic subarachnoid hemorrhage. These results further emphasize the need to establish an early etiological diagnosis and to manage these patients aggressively including early surgery in selected cases.

Aged↗