Dipyridamole plus aspirin versus aspirin alone in secondary prevention after TIA or stroke: a meta-analysis by risk.

OBJECTIVES: To study the effect of combination therapy with aspirin and dipyridamole (A+D) over aspirin alone (ASA) in secondary prevention after transient ischaemic attack (TIA) or minor stroke of presumed arterial origin and to perform subgroup analyses to identify patients that might benefit most from secondary prevention with A+D. DATA SOURCES: The previously published meta-analysis of individual patient data was updated with data from ESPRIT (n = 2,739); trials without data on the comparison of A+D versus ASA were excluded. REVIEW METHODS: A meta-analysis was performed using Cox regression, including several subgroup analyses and following baseline risk stratification. RESULTS: A total of 7612 patients (five trials) were included in the analyses, 3800 allocated to A+D and 3812 to ASA alone. The trial-adjusted hazard ratio (HR) for the composite event of vascular death, non-fatal myocardial infarction and non-fatal stroke was 0.82 (95% confidence interval (CI) 0.72 to 0.92). HRs did not differ in subgroup analyses based on age, sex, qualifying event, hypertension, diabetes, previous stroke, ischaemic heart disease, aspirin dose, type of vessel disease and dipyridamole formulation, nor across baseline risk strata as assessed with two different risk scores. A+D were also more effective than ASA alone in preventing recurrent stroke; HR 0.78 (95% CI 0.68 to 0.90). CONCLUSION: The combination of aspirin and dipyridamole is more effective than aspirin alone in patients with TIA or ischaemic stroke of presumed arterial origin in the secondary prevention of stroke and other vascular events. This superiority was found in all subgroups and was independent of baseline risk.

[Risk of recurrent stroke in adults aged under 45 years following a first ischemic stroke: a five-year study of 95 patients]. / Risque de récidive d'infarctus cérébral chez des adultes jeunes âgés de moins de 45 ans ayant présenté un premier infarctus cérébral. Etude à 5 ans d'une population de 95 patients.

Few data are available concerning the risk of recurrence of cerebral ischemic infarction in young adults (less than 45-years-old) after a first episode of ischemic stroke. From 1992 to 1996, 95 patients less than 45 years old were enrolled in a prospective study in order to define the etiology of their ischemic infarction with systematic and exhaustive explorations. They were recalled five years later (mean follow-up of 67,07 +/- 25,6 months) to determine the risk of stroke recurrence, the rate of cardiac and vascular events and the mortality. At 5 years, 4 patients had a recurrence of ischemic stroke (4.7 p. cent). Seven patients had a coronary event (4 myocardial infarction and 4 angina). Eleven patients died (6 during the acute period). No recurrence of stroke was noticed in patients with stroke of undetermined cause or with minor cardiopathy (abnormalities of the atrial septum). The risk of recurrence of ischemic stroke in young adults appears to be very low.

Chronic inflammatory demyelinating polyneuropathy associated with dysglobulinemia: a peripheral nerve biopsy study in 18 cases.

The possible occurrence of chronic inflammatory demyelinating polyneuropathy (CIDP) in association with an identified dysglobulinemic status is recognized and a causal relationship between the two has been suggested. We had the opportunity to study 18 patients presenting with CIDP and dysglobulinemia. This was an IgG monoclonal gammopathy (IgG MG) in 8 cases, an IgM monoclonal gammopathy (IgM MG) in 8, an IgG-IgM biclonal gammopathy in 1 case and an IgM monoclonal cryoglobulinemia in another. A peripheral nerve biopsy specimen was available for all patients and the morphological findings in these specimens in the cases of CIDP with IgG MG or cryoglobulin did not differ from those without, whereas characteristic features were observed in the cases of CIDP with IgM MG and anti-myelin associated glycoprotein activity.

Serum lipids in young patients with ischaemic stroke: a case-control study.

OBJECTIVES: The relation between serum lipids and ischaemic stroke remains controversial. Studies of lipid related risk factors in cerebrovascular disease have varied greatly in their findings and also in their definition of the cerebrovascular end points. Serum lipids are thought to interact with the pathogenesis of stroke through an atherosclerosis mechanism. Stroke in young patients have been shown to be related to non-atherosclerotic causes most of the time. The aim was to determine the serum lipid profile and the vascular risk factors for ischaemic stroke in a series of patients under 45 with an ischaemic stroke and to compare them with a series of controls of the same age. METHODS: Ninety four consecutive patients with ischaemic stroke were compared with 111 controls of the same age recruited from a regional electoral list. Vascular risk factors were recorded and serum lipid profile was determined in all of them. RESULTS: Multivariate analyses showed that low HDL cholesterol, male sex, smoking, hypertension, and oral contraceptives were risk factors for intracerebral arterial occlusion. CONCLUSION: Low HDL cholesterol was the only serum lipid index to be associated to an increased risk of stroke in this population. Low HDL cholesterol must be considered in the care management of young patients regardless of the detectable presence of atherosclerosis.

[Mechanisms of motor recovery after cerebrovascular accident]. / Mécanismes de la récupération motirce après accident vasculaire cérébral.

Recovery from motor deficit after a stroke remains a puzzling scientific question as well as public health problem. The natural history of deficits after stroke is given to us through published series of patients and we know from them that neurological deficits, spontaneously but most of the time partially, recover. Neuroimaging modern techniques (PET scan, fMRI, evoked potentials) allowed us to identify the main aspects of the post-stroke intracerebral reorganisation. Reorganisation of basal cerebral metabolism, changes in the somatotopia of primary motor cortex, recruitment of remote cortices, participation of associative cortices are clearly part of the rearrangement processes. It is likely that such mechanisms represent the basis of clinical recovery of our patients. However, despite those important advances, very few is known about the effect of treatments on the recovery phenomenon. Some lines of evidence appear now to give rationale to rehabilitation procedures and to drugs suspected to improve clinical recovery.

Cerebral thrombophlebitis in three patients with probable multiple sclerosis. Role of lumbar puncture or intravenous corticosteroid treatment.

We report 3 cases of young patients, 2 women and 1 man, who presented a cerebral venous thrombosis following intravenous treatment with high doses of corticosteroids. All of them presented a probable multiple sclerosis according to clinical, biological (CSF) and MRI criteria and were treated for the first time by a bolus of 1,000 mg of methylprednisolone OD during 5 days. All the usual causes of cerebral venous thrombosis were systematically excluded in all of them. The role of corticosteroid treatment in cerebral thrombophlebitis is discussed. All of them underwent a lumbar puncture a few days before corticosteroid treatment and the relationship between lumbar puncture and cerebral thrombophlebitis is also discussed. Cerebral venous thrombosis associated with corticosteroid treatment has rarely been reported. The relationship between corticosteroids and venous thrombosis has already been suggested but has never been clearly understood.

Fou rire prodromique heralding a left internal carotid artery occlusion.

BACKGROUND: Four rire prodromique, described as pathological laughter preceding the onset of an apoplectic attack, is a rare phenomenon. CASE DESCRIPTION: A 61-year-old man manifested pathological laughter before a sudden right hemiplegia. MRI showed a left lenticular and caudate nucleus infarct with involvement of the external capsule and prerolandic area. MRA revealed a left internal carotid and middle cerebral artery occlusion. CONCLUSIONS: The clinicoanatomic correlates of this phenomenon are discussed.

Impairment and recovery of left motor function in patients with right hemiplegia.

OBJECTIVE: To assess the motor function of the left, supposedly unaffected, limbs of patients with an acute right vascular hemiplegia. METHODS: Fifteen patients with an acute vascular right hemiplegia and 16 matched healthy controls were studied. Motor function of the left limbs of each patient was evaluated on days 20 and 90 after their stroke using four validated tools (hand dynamometer, isokinetic dynamometer, finger tapping, and nine hole peg test). RESULTS: There was a significant impairment of motor function of the left limbs of patients at day 20 compared with controls. The impairment had recovered almost completely at day 90 after the stroke. CONCLUSION: These results show the bilateral cerebral representation of the human motor system and suggest the participation of ipsilateral motor pathways in recovery after a stroke.

[Value of the study of latent atrial vulnerability in unexplained ischemic cerebrovascular accident of young subjects]. / Intérêt de l'étude de la vulnérabilité auriculaire latente dans l'accident vasculaire cérébral ischémique inexpliqué du sujet jeune.

This study searched for abnormalities of the atrial electrophysiological substrate in young subjects with unexplained ischaemic cerebrovascular accidents. Thirty-seven patients (18 to 45 years) underwent programmed atrial stimulation at 2 sites in the right atrium after an unexplained ischaemic cerebrovascular accident. Seventeen of them underwent repeat study at 6 months. The following parameters were analysed: indices of atrioventricular conduction and sinus node automaticity; indices related to atrial hyperexcitability: effective refractory period; adaptation of the refractory periods to heart rate, intraatrial conduction and the index of latent vulnerability; the inducibility test by the extrastimulus technique. The following results were obtained: 54% of patients had an inducible atrial arrhythmia; the effective refractory periods and index of latent vulnerability were lower (204 +/- 21 ms and 2.25 +/- 0.7) in the inducible patients than in the non-inducible patients (232 +/- 28 ms and 3.4 +/- 1.1) (p < 0.001 and p < 0.002 respectively); 76% of patients had latent atrial vulnerability indicating and underlying arrhythmogenic substrate; this substrate was still present 6 months later in 80% of these cases; in patients with an abnormality of the interatrial septum, there was an abnormality of the electrophysiological investigation in 85% of cases compared with 65% in those with normal transoesophageal echocardiography. These results confirm the presence of an arrhythmogenic substrate similar to that of patients with paroxysmal atrial fibrillation in over two thirds of cases. Programmed atrial stimulation is a reproducible technique. The relationship between latent atrial vulnerability and abnormalities of the interatrial septum requires confirmation in a series with a larger numbers of patients.

Recurrent right hemiplegia associated with progressive ipsilateral carotid artery stenosis.

BACKGROUND: Ipsilateral sensory motor symptoms associated with carotid artery stenosis are rare, and few reports are available in the literature. CASE DESCRIPTION: We report the case of a 50-year-old man who presented with right hemiplegia that recurred 14 months later. A left hemisphere watershed infarction was detected. Repeated angiograms showed a left internal carotid occlusion and a right internal carotid stenosis that initially measured 50% and worsened to 80% after the second stroke. CONCLUSIONS: Repeated quantitative measurements of cerebrovascular reserve demonstrated the hemodynamic mechanism of the strokes and the role of a right internal carotid lesion in causing the recurrence of right hemiplegia.

[Ischemic cerebrovascular complications in Rendu-Osler disease: a case]. / Accidents vasculaires cérébraux ischémiques dans le cadre de la maladie de Rendu-Osler: 1 cas.

Rendu-Osler disease is a familial disorder transmitted as an autosomal dominant trait of high penetrance. It is characterized by telengiectasias of the skin, mucous membranes and viscera, associated with recurrent bleedings. Neurological complications (brain abcesses and hemorrhagic manifestations) occur in 10% of the patients. Neurological symptoms are often associated with arteriovenous fistula of the lung (50%). Ischaemic strokes occuring in such patients with an hemorrhagic disease while unfrequent, have been described. The pathophysiology of stroke in that case remains unclear. Polycythemia causing hyperviscosity, air embolism following hemoptysis, paradoxical embolism through right-to-left shunt have been proposed. We report a new case of ischaemic strokes occuring in a caucasian forty-year-old woman, with Rendu-Osler disease (familial history, epistaxis, telengiectasias) and with an arteriovenous malformation of the right lung. She presented two strokes and one transient ischaemic attack. Her pulmonary malformation was occluded by embolization. The role of arteriovenous malformation in the pathophysiology of strokes is discussed.

[Transverse myelitis caused by Mycoplasma pneumoniae infection]. / Myélite transverse induite par une infection à Mycoplasma pneumoniae.

A twenty-six year old man was admitted for febrile atypical pneumoniae. Few hours later, he presented an acute flaccid paraplegia with dorsal pain. Cerebrospinal fluid analysis showed a high leukocyte count with raised protein level. Neuroradiological examinations (myelography and MRI) were normal. Seric immunological disorders were reported. High complement-fixing antibody titers to Mycoplasma pneumoniae were found in the serum and in the CSF. The patient was treated with antibiotic and corticosteroids. He improved dramatically within one month. Neurological complications of Mycoplasma pneumoniae infections have been described (meningoencephalitis, meningitidis, polyradiculoneuropathies, cerebellar ataxia, cranial nerve palsies). Nineteen cases of transverse myelitis induced by Mycoplasma pneumoniae have been previously reported. Pathophysiological mechanisms of nervous system complications induced by Mycoplasma pneumoniae were discussed. Vascular mechanisms, direct invasion by the pathogen, toxic, immunological causes were examined.

The effect of yohimbine on sympathetic responsiveness in essential hypertension.

We have studied the sympathetic response to blockade of presynaptic alpha 2-adrenoceptors in essential hypertension by measuring plasma concentrations of noradrenaline after a single oral dose of yohimbine, an alpha 2-adrenoceptor antagonist. Mean baseline plasma noradrenaline and adrenaline concentrations were similar in the hypertensive and normotensive groups. Yohimbine (0.2 mg x kg-1 orally) caused a lesser increase in the plasma concentrations of noradrenaline in hypertensive patients (+67%) than in normotensive subjects (+178%) and a pressor response in hypertensive (but not in normotensive) patients. These results are consistent with an alteration in the balance of alpha-adrenoceptors (for example presynaptic alpha 2-adrenoceptor desensitization and post-synaptic alpha 1-adrenoceptor hyper-responsiveness) which would help to develop and/or maintain arterial hypertension.

[Is there any desensitization of presynaptic alpha 2-adrenergic receptors in hypertension? Experimental and clinical studies]. / Existe-t-il une désensibilisation des récepteurs alpha 2-adrénergiques présynaptiques dans l'hypertension artérielle? Etudes expérimentales et cliniques.

Several authors have discussed an alteration of adrenergic receptivity in arterial hypertension. De Champlain (Hypertension 1990; 8: S77-S85) suggested that postsynaptic alpha 1-adrenergic functions became dominant while beta-adrenergic functions are attenuated in arterial hypertension. However, the status of presynaptic alpha 2-adrenoceptors remains unknown. The present study investigates presynaptic alpha 2-adrenoceptors in hypertension through the measurement of plasma levels of noradrenaline after administration of yohimbine, an alpha 2-adrenoceptor antagonist, in essential hypertension. Yohimbine (0.2 mg/kg per os) induced a 73% increase of plasma levels of noradrenaline in hypertensive patients (n = 12) and a 178% one in normotensive subjects (n = 6, p < 0.05). A similar significant difference was found in experimental neurogenic hypertension observed in awake dogs 3 weeks after sinoaortic denervation: the increase in plasma concentrations of noradrenaline after yohimbine (0.5 mg/kg i.v.) was +279% in hypertensive versus +642% in normotensive dogs (p < 0.05). The results show that the magnitude of the yohimbine-induced sympathetic activation is lower in hypertensives than in normotensives. They suggest the existence of a presynaptic alpha 2-adrenoceptor desensitization in arterial hypertension. The abnormality of this presynaptic inhibitory mechanism can increase the sympathetic tone and help to develop and maintain arterial hypertension.

SPECT study of cerebral blood flow reactivity after acetazolamide in patients with transient ischemic attacks.

We investigated 15 patients with one or more transient ischemic attacks (TIAs) in the internal carotid artery territory within the month following the most recent TIA. Cerebral blood flow (CBF) was measured by single-photon emission computed tomography, using intravenous xenon-133 before and after injection of 1 g acetazolamide. Six patients had severe carotid stenosis or occlusion; the other nine patients had no significant carotid lesions. Twenty age-matched volunteers free of neurologic symptoms or history were used as controls. Mean CBF in the sylvian region was not significantly different between patients and controls. Seven patients exhibited a focal hypoperfusion at rest in the symptomatic hemisphere, and their hypoperfused areas were hyporeactive after administration of acetazolamide. Seven other patients exhibited hyporeactive areas after acetazolamide administration while their CBF tomograms at rest were normal. Thus, CBF abnormalities were detected in 14 of the 15 patients. Our findings suggest that CBF measured early after acetazolamide administration could be useful to confirm the clinical diagnosis of TIA. In the nine patients with no significant lesion of the internal carotid artery, the areas of hypoperfusion were small and were probably related to the focal ischemic event. In the six patients with severe lesions of the internal carotid artery, abnormalities were of variable size and intensity but were often large and pronounced. The discrepancy between these two subgroups of patients could be ascribed to the hemodynamic influence of the internal carotid artery lesions. Moreover, our findings may provide some insight into the pathophysiology of TIAs.