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J Montaner

Publications and source records attributed to J Montaner.

66 records · Page 4Linked to original sources

[Vertebrobasilar abnormalities in patients with hemifacial spasm: MR-angiography findings].

INTRODUCTION: Hemifacial spasm (HFS) is a disorder characterized by a complex of symptoms with hyperactive motor dysfunction of the facial nerve. It is indicated that HFS in the majority of cases can be caused by a blood vessel compressing the nerve adjacent to the brainstem. PATIENTS AND METHODS: We studied and treated 44 patients with HFS. Magnetic resonance imaging (MR) and MR-angiography of the brain were performed in patients with HFS to asses the presence of an artery of the vertebrobasilar system compressing the root of the facial nerve. We evaluate the response to treatment with Botulinum toxin in these cases. 14 patients were excluded (6 patients presented HFS due to other lesions and in 8 patients the MR was not performed). The remaining 30 patients with idiopathic HFS underwent MR/MRA (3D-FISP) and it was also performed in 14 patients with synkineses after facial palsy to be used as controls. RESULTS: The MRA documented an abnormal position of the arteries surrounding the facial nerve (ipsilaterally to HFS) in 22 patients. The compressing artery was the PICA in 3 patients (10%), the AICA in 3 patients, the vertebral artery in 7 patients and the basilar artery in 8 patients, one patient showed a combined compression by AICA and PICA. The remaining 8 patients had a normal MRI. At the control group only one patient presented an abnormal AICA and the other had a normal MRI-MRA. Patients were followed-up for 22.4 months and after Botulinum toxin treatment patients kept 4.81 months free of symptoms. CONCLUSIONS: We recommend to perform MR studies in all HFS patients to rule out a secondary cause of the disease and MRA to evaluate the underlying vertebrobasilar abnormalities if surgery is planned. Botulinum toxin is a useful treatment in these patients and only after its failure, microvascular decompression will be considered.

Basilar Artery↗

[Determination of Doppler parameters in the study of basal cerebral veins: basal vein of Rosenthal and middle cerebral vein].

INTRODUCTION: To date, little attention has been paid to the study of the venous system by means of transcranial Doppler ultrasound. The objective of our study was to learn how to localize cerebral blood flow and find the normal values of different ultrasonographic parameters. PATIENTS AND METHODS: We studied 20 healthy persons in whom the arterial system of the circle of Willis had previously been shown to be normal. Transcranial Doppler scan was done with the person lying face upwards, using a transtemporal 2 MHz catheter. In the study we included persons in whom at least one of the two veins could be studied unilaterally. RESULTS: We studied twelve men and eight women aged between 25 and 78 years. The basal vein of Rosenthal, localized bilaterally in 70% of the cases, was identified as a wave of low pulsation between segments P1 and P2 of the posterior cerebral artery, going away from the catheter at a speed of about 11 cm/second. The middle cerebral vein was found bilaterally in only 35% of the cases as a wave near to the middle cerebral artery but in the opposite direction, at an average velocity of approximately 11.7 cm/second and of low pulsation. CONCLUSIONS: In spite of the technical problems, which can be solved using contrast agents, it is possible to study the cerebral venous system by means of transcranial Doppler. Our Unit is the first in Spain to show this. We therefore wish to promote the use of transcranial Doppler in cerebral venous disorders.

Adult↗

[Acute pseudobulbar paralysis: the use of diffusion techniques with magnetic resonance].

INTRODUCTION: Acute pseudobulbar palsy produced by bilateral cerebral infarctions is a rare syndrome, which includes among its symptoms mutism, severe dysphagia and diverse sensory-motor signs. CLINICAL CASES: We report two middle-aged patients who suddenly developed a severe dysarthria and dysphagia, which impeded their ability to speak and to feed themselves, with spasmodic laughing and crying and slight motor deficit ('pure' pseudobulbar palsy). The acute lesions, using conventional and diffusion-weighted magnetic resonance imaging, corresponded partially to the anterior choroidal artery (case 1: acute lesion in the left periventricular white matter and a subacute one in the right semioval centrum; case 2: acute lesions in the right frontal subcortical white matter and in the periventricular white matter adjacent to the left lateral ventricle). The favorable evolution of these patients in contrast to previously described patients with acute pseudobulbar palsy could indicate that the motor deficit is a prognostic factor for this syndrome. CONCLUSIONS: Diffusion-Weighted magnetic resonance imaging permits differentiation with high precision of the acute lesions in patients who present old ones. Sometimes multiple acute lacunar infarctions (MALI) are found to be responsible of the syndrome. Hypertension and diabetes are the risk factors for the small vessel disease underlying these MALI.

Acute Disease↗

[Lack of correlation between plasma homocysteine levels and cerebral microangiopathy in patients wtih transient ischemic attack].

OBJECTIVE: The aim of this study is to evaluate cerebral MRI findings in patients with atherothrombotic transient ischemic attacks (TIA) and its correlation with plasma homocysteine (Hcy) levels. PATIENTS AND METHODS: A total of 62 consecutive patients with the diagnosis of TIA of atherothrombotic origin were studied. MRI examinations were performed in all patients for the evaluation of the presence of infarct and/or white matter hyperintensities (WMHI). Plasma Hcy levels were determined according to the method described by Smolin and Schneider modified. RESULTS: Plasma Hcy levels were significantly (p < 0.036) higher in patients with MRI-detected infarcts (9.69 +/- 2.06 mumol/l) compared with patients without infarcts (8.65 +/- 1.7 mumol/l. There was no correlation (p < 0.33) between plasma Hcy levels and the presence or absence of WMHI seen on MRI. CONCLUSIONS: In TIA patients, plasma Hcy levels were significantly higher in patients with cerebral infarcts, but did not correlate with the presence of WMHI. Our results suggest that mild hyperhomocysteinemia would be associated with large-medium vessel rather than with small vessel disease.

Adult↗

[Diffusion-weighted magnetic resonance in the diagnosis of acute subcortical infarcts].

INTRODUCTION: The diagnostic efficacy of radiological studies in acute subcortical infarcts is limited by the low sensitivity of conventional computerized tomography (CT) and magnetic resonance (MR) in detecting small-sized infarcts, and the difficulty in differentiating acute from chronic lesions. Diffusion-weighted MR (DMR) has shown great sensitivity and specificity in the detection of small vessel ischemic lesions during the acute phase. OBJECTIVE: To determine the diagnostic value of DMR in the study of patients with subcortical infarcts during the acute phase. PATIENTS AND METHODS: We made a prospective analysis of 100 consecutive patients with a clinical diagnosis of subcortical infarct. In all cases MR examination was done within the first 10 days (average 3.9 days) following onset, using conventional and diffusion-weighted sequences. RESULTS: In all cases the DMR showed the presence of ischemic lesions which explained, at least partly, the clinical features of the stroke. In 42 patients (42%) the DMR gave relevant information for diagnosis, as compared with the conventional MR studies, by confirming the presence of an ischemic lesion responsible for the clinical picture. The percentage rose to 50% when the examination was done within the first two days. CONCLUSIONS: DMR gives useful information in a high percentage of patients with acute subcortical infarcts. This is due to its great sensitivity in the detection of acute lesions of small size, and capacity to distinguish acute from chronic lesions.

Acute Disease↗

[Correlation between the expression of proinflammatory cytokines and matrix metalloproteinases in the acute phase of an ischemic stroke].

INTRODUCTION: Proinflammatory cytokines are the main responsible for the onset of postischemic inflammatory cascade. Recently, the deleterious effect of matrix metalloproteinases (MMPs) in the acute phase of stroke has been described. Animal models suggest a link between both families. OBJECTIVE: We aimed to investigate possible relations between the MMP overproduction and proinflammatory cytokine expression after human ischemic stroke. PATIENTS AND METHODS: From all consecutive stroke patients attended during a 10 months period, we selected and prospectively studied those presenting as a cardioembolic stroke involving the MCA territory. MMP 9, MMP 2 and IL 6 were serially measured by means of ELISA at study entry and at 12, 24 and 48 hours after symptoms onset. RESULTS: A total of 39 patients were studied. A positive correlation was found between mean expression of both MMPs and IL 6 (r= 0.33, p= 0.040 for MMP 2 y r= 0.45, p= 0.004 for MMP 9). From all measured timepoints, the best obtained correlation was that of MMP 9 with IL 6 at 24 hours (r= 0.418, p= 0.010). At 24 h a peak value of IL 6 was observed. Baseline MMP 2 and MMP 9 levels showed a trend to correlate with that peak of IL 6 (r= 0.329, p= 0.061 for MMP 2 y r= 0.325, p= 0.061 for MMP 9). CONCLUSION: MMP expression correlates with the inflammatory cascade activation after acute cardioembolic stroke.

Acute Disease↗

[Chronic subdural hematoma simulating a TIA. Implications for the management transient neurological deficit].

Chronic subdural hematoma that generally happens after cranial trauma doesn't have clinical manifestations until days or weeks after the traumatism. Due to the lesions nature, symptoms are almost always progressive and presentation as transient ischemic attacks (TIA) is very uncommon. We describe 2 cases of chronic subdural hematoma that started simulating TIA and we discuss its implications in the management of those patients who had presented transient neurological deficit.

Aged↗

[Role of homocysteine in the acute phase of stroke].

INTRODUCTION: Hyperhomocysteinemia is a well known vascular risk factor. However its action mechanism and its role in the acute phase of stroke have not been determined. OBJECTIVES: To study plasmatic homocysteine levels in the acute stroke of different etiologies and evaluate its role as a prognostic factor. METHODS: We determined plasmatic homocysteine in 136 consecutive patients with stroke. Mean time from symptoms onset was 4.6 hours. RESULTS: Higher than normal homocysteine levels were found in ischemic stroke (n= 119 13.1 micromol/l; 43 % of patients > normality rank) and intracranial hemorrhage (n= 17 micromol/l; 24 % of patients > normality rank). The etiological distribution of ischemic stroke was the following: 42 cardioembolic (29.4%; median Hcy: 13.1 micromol/l), 20 atherothrombotic (14 %; Hcy: 12.7 micromol/l), 33 lacunar (23.1 %; Hcy: 11.8 micromol/l) and 24 undetermined (16.8%; Hcy:15.2 micromol/l). No significant differences were found between these groups (p=0.19). Those patients who presented early neurological deterioration presented higher homocysteine levels than those who remained stable or improved (median 13.3 n=16 v 11.3 n=113; p=0.061). CONCLUSIONS: High homocysteine levels are associated to all etiologic stroke subtypes and intracranial hemorrhage. Patients who experienced early neurological worsening tend to have higher homocysteine levels.

Acute Disease↗

[Clinical factors predicting the appearance of vascular events following a transient ischemic attack].

INTRODUCTION: Patients who have suffered a transient ischemic attack (TIA) have a high risk of undergoing a severe vascular event. Most of them do not receive early attention and cannot benefit from an adequate diagnosis and treatment. AIMS: The aim of this study is to identify the clinical factors that predict the appearance of a new vascular event in these patients. PATIENTS AND METHODS: We conducted a prospective study of 104 TIA patients, who had been given attention during the first 24 hours after the onset of symptoms, for a mean follow up time of 12.6 months. RESULTS: The incidence rates of strokes, ischemic heart disease, peripheral arteriopathy and death were 13, 6, 3 and 8%, respectively. Multivariate analysis identified the following aspects as independent predictors of new strokes: an age above 73 odds ratio (OR) 4.46 (CI 95%, 1.15 17.38) and an atherothrombotic aetiology OR 4.36 (CI 95%, 1.4413.18); and episodes of ischemic heart disease, a history of suffering from such heart disease OR 30.65 (CI 95%, 2.94319.17) and taking oral antidiabetic drugs OR 31.23 (CI 95%, 2.65368.74). Leukocytosis OR 11.21 (CI 95%, 1.25100.39) is linked to the deaths caused by vascular disorders, whereas an atherothrombotic aetiology OR 3.83 (CI 95%, 1.31 11.20) and being male OR 3.44 (CI 95%, 1.02 11.60) were seen to be predictors of the appearance of any vascular event. CONCLUSIONS: Our findings showed that the risk of suffering severe vascular events after a TIA becomes higher. There are a number of useful clinical variables (age above 73, atherothrombotic aetiology, being male, taking oral antidiabetic drugs and leukocytosis) for identifying the patients at the highest risk.

Age Factors↗

[Angiogenesis in human cerebral ischemia].

OBJECTIVE: We aimed to review current knowledge about angiogenesis processes following stroke and possible benefit of future therapeutic angiogenic-related treatments. DEVELOPMENT: Angiogenesis is a physiopathologic process where new vessels arise from pre-existing ones within different phases: sprouting and maturation. To modulate angiogenesis there is a balance between several promoters like VEGF, bFGF, MMPs, etc. but also with inhibitors or angiostatic molecules such as angiostatin, endostatin, etc. In human pathologies angiogenesis has a dual effect: useful in wound healing, tissue remodelling or ischemic heart disease but harmful in cancer, rheumatoid arthritis or atheroma plaque instability and rupture. Angiogenesis is involved in some cerebrovascular diseases. Following ischemic stroke there is an overexpression of several molecules related with this process, although its finality remains largely unknown. CONCLUSION: Angiogenesis is activated after stroke modifying capillary network. To obtain advantages from angiogenesis, it will be essential to achieve the temporal profile of these molecules in humans, and to investigate if its effects are different in acute or chronic stroke phases. In the future, angiogenesis modulation could take part of a combined stroke therapy.

Angiogenesis Inhibitors↗

[Neurological manifestations of Fabry disease].

AIM: To present a review of the neurological manifestations, diagnosis and treatment of Fabry disease. DEVELOPMENT: Fabry disease is a hereditary deficiency of lisosomal alpha-galactosidase A resulting in accumulation of globotriaosylceramide in vascular endothelium and smooth-muscle cells. Neurological manifestations include severe attacks of neuropathic pain and acroparesthesias at early age and small-vessel occlusive disease in adults. Other manifestations are renal dysfunction, cardiomyopathy, abdominal pain, deafness, angiokeratoma and corneal opacity. Cerebrovascular involvement results from small-arteries lipid deposition, impairment in cerebrovascular reactivity, vertebrobasilar ectasia as well as vascular risk factors such as nephrogenic hypertension and cardiac disease. Fabry disease prevalence seems to be higher than previously described and currently many patients might be underdiagnosed. CONCLUSIONS: Fabry disease must be included in the differential diagnosis of stroke in young people, particularly in those with criptogenic etiology, vertebrobasilar location and renal dysfunction. The diagnosis has important therapeutic implications since it is available a replacement therapy with agalsidase, a recombinant enzyme which has been effective in lipid tissue clearance and clinical improvement in Fabry patients.

Adolescent↗