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M Ossemann

Publications and source records attributed to M Ossemann.

6 recordsLinked to original sources

[Tropical spastic paraparesis due to HTLV-I. 4 case reports and literature review].

We describe the clinical, radiological, neurophysiological and biological characteristics of 4 patients suffering from tropical spastic paraparesis due to a HTLV-I infection. Patient 1 immigrated in Europe at the age of 16 from Caribbean islands. Patient 2 was a White male Caucasian who lived during several years with a prostitute also native of Caribbean islands. Patient 3 was a Black male Zaïrian and Patient 4 was a female of mixed race who lived many years in Zaäire and in Senegal. All the 4 patients presented with walking difficulties, a spastic paraparesis, urinary disturbances and often, severe constipation. The diagnosis was based on a positive ELISA test for HTLV-I antibodies, confirmed in 2 cases each by Western blots and detection of the viral genome by the Polymerase Chain Reaction. In all cases, CSF pleocytosis and CSF-restricted oligoclonal IgG bands were observed. MRI of the spinal cord showed a global atrophy in 3 cases. Cerebral MRI revealed unusual extensive, progressive and symmetric lesions of the white matter in Patient 1, and some patchy periventricular lesions in Patient 4; this examination was normal in the two other cases. Sensory evoked potentials indicated abnormalities of central conduction velocities at the level of the posterior columns. The pathogenesis of tropical spastic paraparesis is briefly discussed.

Aged

Association between stroke and atrial septal aneurysm assessed by transesophageal echocardiography in a cardiologic population.

Atrial septal aneurysm (ASA) is now recognized as a source of emboli. Its prevalence in a general population remains controversial. We assessed, in a cardiologic population, the prevalence of ASA, the association with cerebrovascular events, the role of associated interatrial shunting and age. Four hundred and ninety-four consecutive patients were referred for transesophageal echocardiography with contrast. The prevalence of ASA in two groups, with (A) and without (B) cerebrovascular events were compared. In group A, we studied the prevalence of ASA according to the clinical presentation (stroke, TIA and peripheral emboli in limbs). An ASA was found in 38 patients (8%). The prevalence of ASA was higher in group A (16%) than in group B (4%) (p < 10(-5)). Prevalence of ASA was not significantly different in stroke, TIA and peripheral emboli subgroups. There was no difference in prevalence of ASA in stroke or TIA subgroups according whether age was < 55 years or > or = 55 years. Prevalence of all types of vascular events was increased when ASA was associated with an interatrial shunt. Our results support the assumption that ASA is a potential source of cerebrovascular events, whatever the clinical presentation or age. Presence of interatrial shunt increases the risk of stroke in subjects with ASA.

Adult

Stroke subtypes and risk factors associated with silent infarctions in patients with first-ever ischemic stroke or transient ischemic attack.

The relationship between the presence of silent cerebral infarcts (SCI) and etiology of an acute cerebral ischemia remains controversial. In a population of 306 patients with a first-ever stroke (225) or transient ischemic attack (TIA) (81), we studied the prevalence and associated risk factors of SCI as well as the presumed etiology of the qualifying event. Silent infarction was defined as a focal hypodensity on brain CT, not related to the recent ischemic event. The overall prevalence was 33% (102/306) with a higher rate in stroke patients (83/225, 37%) than in TIA patients (19/81, 23%; p = 0.028). Age (p < 0.01), smoking (p < 0.01), hypertension (p = 0.013), and leukoaraiosis (p = 0.05) were significantly associated with SCI, but only in some degree in TIA patients. Presence of SCI was statistically associated with a small-artery disease (p < 0.01) considered as the cause of the qualifying event. Emboligenic cardiopathy was significantly more frequent in patients without SCI (p < 0.05) in the TIA subgroup. Thus, in patients with silent cerebral infarcts, small-vessel disease may be in most cases the cause of the recent symptomatic cerebral ischemia.

Aged