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Biomedical subjects

J L Mas

Publications and source records attributed to J L Mas.

At least 55 records · Page 3Linked to original sources
PubMed1998

[Cerebral infarction: a diagnostic and therapeutic emergency].

Emergency management of cerebral infarct aims to confirm the diagnosis, determine the mechanism and the cause (on which depend the prognosis and treatment), prevent and treat immediate, general and neurologic complications and to begin as early as possible the appropriate treatment. A first progressive step was made with the creation of hospital units devoted to management of cerebrovascular accidents. Various studies showed that patients hospitalised in such units have not only better survival and functional prognosis, but also that the length of hospitalisation and the number of patients requiring subsequent hospitalisation in rehabilitation centres are significantly reduced. More recently, clinical trials suggested that thrombolytic treatment, although comprising a risk of severe cerebral haemorrhage, can clearly improve patient prognosis if it is given in the first hours. Cerebral infarct should henceforth be considered as a medical emergency, and our health care system should be adapted to give patients the best chance of cure.

Cerebral Infarction↗
PubMed1998

[Prevention of cerebral infarct caused by atherosclerosis].

Atherosclerosis of the cerebral arteries is the main cause of cerebral infarction but the frequency with which this cause is implicated is very variable from one trial to another depending on the criteria used. Primary prevention of this type of infarction is mostly based on the correction of arterial risk factors and on carotid artery surgery in selected cases. Aspirin does not appear to the effective in this indication. The respective indications of heparin and aspirin in the acute phase of cerebral infarction remain controversial despite the recent publications of large scale therapeutic trials. The benefits of these treatments is, at best, globally modest. Thrombolytics could, on the other hand, revolutionize the treatment of acute cerebral infarction if the encouraging results of a recent trial using rt-PA in the first 3 hours, are confirmed by other trials. After the acute phase, antiplatelet agents (aspirin, ticlopidine, clopidogrel or aspirin associated with dipyridamole) and surgery in patients with symptomatic carotid artery stenosis greater than 50% or 70-80% (according to the method of measurement) have been shown to be effective. Several large scale trials are under way to assess the benefits and risks: a) of antihypertensive therapy in patients with previous cerebrovascular accidents, b) of treatment with statins of patients at high risk of infarction due to atherosclerosis, c) of oral anticoagulants at low dosage (versus antiplatelet agents) in secondary prevention, d) of thrombolytics in the acute phase of cerebral infarction, e) of carotid angioplasty (versus surgery) in patients with symptomatic severe stenosis.

Arteriosclerosis↗
PubMed1997

Adie syndrome as the initial sign of primary Sjögren syndrome.

PURPOSE: To report Adie syndrome as the initial sign of primary Sjögren syndrome. METHODS: Case report. RESULTS: Adie syndrome was associated with necrotizing gingivitis and xerostomia. Antibodies against Ro (SS-A) were present. Prednisone and antimalarial drugs were ineffective in treating Adie syndrome but improved the necrotizing gingivitis. CONCLUSION: Search for Sjögren syndrome is mandated in patients with Adie syndrome. The latter condition is likely related to ganglionitis, a mechanism responsible for peripheral nervous system involvement in primary Sjögren syndrome.

Adie Syndrome↗
PubMed1997

Arterial ischemic strokes associated with pregnancy and puerperium.

Physiological changes occurring during pregnancy and puerperium may increase the risk of stroke. However, the incidence rate of ischemic stroke is of 3.8 to 5 in 100,000 pregnancies, i.e. quite similar to that of ischemic strokes occurring in non pregnant women of child bearing age. Whereas eclampsia, choriocarcinoma and amniotic emboli occur only during pregnancy or puerperium, peripartum cardiomyopathy and benign cerebral angiopathy are less specific. All other causes of cerebral ischemia may also occur during pregnancy and puerperium. The management of an ischemic stroke should not differ between pregnant and non pregnant women of child bearing age. Strokes associated with pregnancy require a complete diagnostic work-up including angiography if necessary. Low doses of aspirin (60-80 mg/d) can be used after 3 months of pregnancy. Heparin is the anticoagulant of choice during pregnancy, but warfarin may be used between 13 and 36 weeks of gestation; heparin and warfarin can be used during breast feeding. There is no neurological reason to recommend a systematic use of cesarean section. Subsequent prescription of oral contraceptive therapy is not recommended except in patients with a definite cause of ischemic stroke which is not influenced by hormones.

Arterial Occlusive Diseases↗
PubMed1997

[Extensive cerebral venous thrombosis resistant to heparin: local fibrinolysis with urokinase].

A 37 year-old man had headaches for 10 days, then a single tonic-clonic seizure and coma due to an extensive cerebral venous thrombosis. In spite of full-dose heparin treatment for 7 days, the clinical picture worsened along with increasing edema on CT-Scan. Direct thrombolytic treatment was then performed using transvenous catheterization and instillation of Urokinase (2.6 MU over 4 days). A near complete repermeabilization of the sinuses was obtained and the patient improved dramatically in a few days. The only adverse effect of Urokinase was hematuria. Based on our experience and review of the literature which includes 26 previous cases, direct thrombolytic therapy appears to be a relatively safe procedure. This treatment should be considered in a patient with extensive dural sinus thrombosis which fails to respond to heparin treatment.

Adult↗
PubMed1997

[Simultaneous supratentorial multiple cerebral infarctions].

We assessed the frequency, clinical and etiological correlates of acute supratentorial multiple infarcts from a hospital-based prospective stroke registry. Among 383 consecutive patients admitted with acute supratentorial infarcts, 352 had single infarcts and 31 (8.1 p. 100) had multiple infarcts on computed tomography. Multiple infarcts were bilateral in 18 patients and unilateral in 13 patients. In only one third of cases, could the diagnosis of multiple infarcts be suspected clinically before neuroimaging. Compared with patients with acute supratentorial single infarcts, the 18 patients with bilateral acute supratentorial multiple infarcts were younger and had a special etiological profile. Indeed, an unusual definite cause of stroke was identified in 8 of them, including coagulopathy/systemic disorders or rare non-atherosclerotic arteriopathy. Major cardiac sources of embolism were identified in 4, whereas large artery artherosclerosis accounted for only 2 cases. In 3 cases, uncertain causes (abnormalities whose link to stroke could not be clearly established) were found. The etiological workup was entirely negative in one. The 13 patients with unilateral acute supratentorial multiple infarcts did not differ significantly from those with acute supratentorial single infarct, concerning age, gender and risk factor profile. In 7 of them, the infarcts involved the anterior circulation (with or without associated posterior borderzone infarct). Six had ipsilateral ICA disease and one a major cardioembolic source associated with coagulopathy. In the other 6 patients, the infarcts involved the anterior and posterior circulations. Three had a major cardiac source of embolism and one a multifocal intracranial angiopathy. The cause of stroke was uncertain in one patient and the etiological workup was entirely negative in another. In conclusion, acute supratentorial multiple infarcts are not rare (8.1 p. 100). A minority of patients (32 p. 100) had a clinical picture suggesting multiple infarction. Some topographic patterns were associated with etiological correlates: unusual causes of stroke (coagulopathy/systemic disorders) and cardioembolism in bilateral acute supratentorial multiple infarcts; ipsilateral ICA disease in unilateral acute supratentorial multiple infarcts involving the anterior circulation (with or without associated posterior bordezone infarct): cardioembolism in unilateral supratentorial multiple infarcts involving the anterior and posterior circulations.

Cerebral Infarction↗
PubMed1996

A reversible posterior leukoencephalopathy syndrome.

BACKGROUND AND METHODS: In some patients who are hospitalized for acute illness, we have noted a reversible syndrome of headache, altered mental functioning, seizures, and loss of vision associated with findings indicating predominantly posterior leukoencephalopathy on imaging studies. To elucidate this syndrome, we searched the log books listing computed tomographic (CT) and magnetic resonance imaging (MRI) studies performed at the New England Medical Center in Boston and Hôpital Sainte Anne in Paris; we found 15 such patients who were evaluated from 1988 through 1994. RESULTS: Of the 15 patients, 7 were receiving immunosuppressive therapy after transplantation or as treatment for aplastic anemia, 1 was receiving interferon for melanoma, 3 had eclampsia, and 4 had acute hypertensive encephalopathy associated with renal disease (2 with lupus nephritis, 1 with acute glomerulonephritis, and 1 with acetaminophen-induced hepatorenal failure). Altogether, 12 patients had abrupt increases in blood pressure, and 8 had some impairment of renal function. The clinical findings included headaches, vomiting, confusion, seizures, cortical blindness and other visual abnormalities, and motor signs. CT and MRI studies showed extensive bilateral white-matter abnormalities suggestive of edema in the posterior regions of the cerebral hemispheres, but the changes often involved other cerebral areas, the brain stem, or the cerebellum. The patients were treated with antihypertensive medications, and immunosuppressive therapy was withdrawn or the dose was reduced. In all 15 patients, the neurologic deficits resolved within two weeks. CONCLUSIONS: Reversible, predominantly posterior leukoencephalopathy may develop in patients who have renal insufficiency or hypertension or who are immunosuppressed. The findings on neuroimaging are characteristic of subcortical edema without infarction.

Adolescent↗
PubMed1996

Phenotype of autosomal dominant spastic paraplegia linked to chromosome 2.

We report the clinical features of 12 families with autosomal dominant spastic paraplegia (ADSP) linked to the SPG4 locus on chromosome 2p, the major locus for this disorder that accounts for approximately 40% of the families. Among 93 gene carriers, 32 (34%) were unaware of symptoms but were clinically affected. Haplotype reconstruction showed that 90% of the asymptomatic gene carriers presented increased reflexes and/or extensor plantar responses independent of age at examination. The mean age at onset was 29 years, ranging from 1 to 63 years. Intra- as well as inter-familial variability of age at onset was important, but did not result from anticipation. Phenotype-genotype correlations and comparison with SPG3 and SPG5 families indicated that despite the variability of age at onset, SPG4 is a single genetic entity but no clinical features distinguish individual SPG4 patients from those with SPG3 or SPG5 mutations.

Adolescent↗
PubMed1996

Diagnosis and management of paradoxical embolism and patent formen ovale.

Recent investigations of patients with cerebral and peripheral arterial emboli of unknown cause suggest that paradoxical embolism through a patent formen ovale (PFO) might be responsible for more arterial embolic events than previously realized. In most cases, however, a causal relationship between the embolic process and the PFO cannot be established with certainty. The presumptive nature of the clinical diagnosis of paradoxical embolism together with the lack of precise data on the risk of recurrent embolization do not facilitate the proper treatment of these patients. In the rare case of proved paradoxical embolism with a thrombus straddling a PFO discovered by echocardiography, the available literature suggest that embolectomy and closure of the PFO is the most logical approach. The long-term treatment of patients with presumed paradoxical embolism is controversial. Further studies are needed to assess the risk of recurrent arterial ischemic events associated with PFO, to determine which patients are at increased risk of recurrent events, and to assess the potential benefits from various therapeutic interventions (anticoagulants or antiplatelet drugs, surgical or transcatheter closure of the PFO). Otherwise, we risk exposing these patients to unnecessary treatment complications.

Embolism, Paradoxical↗
PubMed1996

Factor V Leiden mutation in cerebral venous thrombosis.

BACKGROUND AND PURPOSE: Resistance to activated protein C is a common inherited risk factor for venous thrombosis, which is due to a mutation in coagulation factor V (factor V Leiden mutation). It is present in approximately 20% of unselected consecutive patients with deep vein thrombosis. The rate of resistance to activated protein C in patients with cerebral venous thrombosis (CVT) is unknown. METHODS: We investigated the association of factor V mutation with CVT using a case-control study. Nineteen unselected patients with CVT and 57 healthy control subjects were tested for the point mutation. RESULTS: The mutation was found in a heterozygous form in 4 of the 19 patients with CVT (21%) and in only 1 of the 57 control subjects (2%) (P = .02, Fisher's exact test). The prevalence of the coagulation defect found in our patients with CVT was consistent with that observed in previous studies in patients with deep vein thrombosis. In 3 of the 4 patients positive for the mutation, CVT developed in the presence of an acquired prothrombotic state, including oral contraceptive use in 2 patients and puerperium in the third. CONCLUSIONS: Factor V Leiden mutation is a risk factor for CVT and may be the most common inherited coagulation defect associated with this condition.

Adult↗
PubMed1996

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, genetic homogeneity, and mapping of the locus within a 2-cM interval.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a recently identified autosomal dominant cerebral arteriopathy characterized by the recurrence of subcortical infarcts leading to dementia. A genetic linkage analysis conducted in two large families recently allowed us to map the affected gene on chromosome 19 in a 12-cM interval bracketed by D19S221 and D19S215. In the present study, these first 2 families and 13 additional ones, including a total of 199 potentially informative meiosis, have been genotyped with eight polymorphic markers located between D19S221 and D19S215. All families were linked to chromosome 19. The highest combined lod score (Zmax = 37.24 at theta = .01) was obtained with marker D19S841, a new CAn microsatellite marker that we isolated from chromosome 19 cosmids. The recombinant events observed within these families were used to refine the genetic mapping of CADASIL within a 2-cM interval that is now bracketed by D19S226 and D19S199 on 19p13.1. These data strongly suggest the genetic homogeneity of this recently identified condition and establish the value of its clinical and neuroimaging diagnostic criteria. Besides their importance for the ongoing positional cloning of the CADASIL gene, these data help to refine the genetic mapping of CADASIL relative to familial hemiplegic migraine and hereditary paroxysmal cerebellar ataxia, conditions that we both mapped within the same chromosome 19 region.

Cerebral Arterial Diseases↗
PubMed1996

[Patent foramen ovale, aneurysm of the interatrial septum and cerebral ischemic complication].

Persistence of a patent foramen ovale (PFO) and the presence of an aneurysm of the interatrial septum (AIAS) are significantly more frequent in patients examined for cerebral ischaemic accident of unknown cause than in control subjects. The mechanism of ischaemic accidents associated with these cardiac abnormalities (frequently associated with each other), particularly the frequency of paradoxical embolism, remains unclear. In young patients, the risk of recurrent cerebral ischaemic accident appears to be generally low (1 to 2% per year). Secondary prevention remains empirical and controversial. No comparative studies are available to demonstrate the superiority of platelet antiaggregants, oral anticoagulants or invasive treatments, such as endovascular or surgical closure of the foramen ovale. A rational treatment can only be proposed on the basis of a better understanding of the natural history of ischaemic recurrences (identification of subgroups of patients at high or low risk of recurrence) and the therapeutic benefit risk ratio.

Brain Ischemia↗
PubMed1995

Recurrent cerebrovascular events in patients with patent foramen ovale, atrial septal aneurysm, or both and cryptogenic stroke or transient ischemic attack. French Study Group on Patent Foramen Ovale and Atrial Septal Aneurysm.

Patent foramen ovale (PFO) and atrial septal aneurysm (ASA) have been identified as potential risk factors for stroke, but information about the risk of recurrent cerebral ischemia is scarce. The aim of this retrospective study was to assess the absolute risk of recurrent cerebrovascular events in 132 patients under 60 years of age with patent foramen ovale, atrial septal aneurysm (diagnosed by transesophageal echocardiography with a contrast study), or both and an otherwise unexplained stroke or transient ischemic attack (TIA). During a mean follow-up of 22.6 +/- 16 months, six patients had a recurrent stroke (n = 2) or a TIA (n = 4). No systemic embolism was observed. The actuarial risk of having a recurrent stroke was 2.3% (95% confidence interval, 0.6% to 8.2%) at 2 years, whereas the risk of having a stroke or a TIA was 6.7% (95% confidence interval, 3.1% to 14.2%) at 2 years. The average annual rates of recurrence were 1.2% and 3.4%, respectively. In patients with both PFO and ASA, the actuarial risk of a first recurrent stroke was 9.0% (95% confidence interval, 2.4% to 28.5%) at 2 years, with an average annual rate of recurrence of 4.4%. As a group, patients with patent foramen ovale, atrial septal aneurysm, or both and an otherwise unexplained stroke or TIA appear to have a low risk of recurrent stroke whatever the prophylactic antithrombotic therapy used. The association of ASA and PFO may be an indicator of a higher risk of recurrent stroke.

Adult↗