Acute myelitis as presenting symptom of HIV-HTLV-1 co-infection.

A 21-year-old woman presented with acute-onset spastic paraparesis. The MRI spinal scan revealed a contrast-enhanced T2 hyperintensity between C5-T2. The most common neurotropic pathogens were excluded by first level tests. Under suspicion of an acute immune-mediated myelitis, a corticosteroid therapy was administered. However, a seropositivity for both human immunodeficiency virus (HIV) type 1 and human T-lymphotropic virus (HTLV) subsequently emerged. An antiretroviral therapy was started while steroids discontinued. Patient's clinical conditions remained unchanged. HIV-HTLV-1 co-infection should be included in the differential diagnosis of any acute myelitis, even in patients with a preserved immune status and no risk factors.

Amino acid supplementation in l-dopa treated Parkinson's disease patients.

BACKGROUND: The correlation between Parkinson disease and malnutrition is well established, however a protein-restricted diet is usually prescribed because of potentially negative interactions between dietary amino acids and l-dopa pharmacokinetics. This strategy could increase the risk of further nutritional deficits. METHODS: A monocentric, prospective, randomized, double-blind pilot study was performed on two groups of Parkinson-affected, protein-restricted, patients: Intervention (n = 7; amino acid supplementation twice daily) and Placebo (n = 7; placebo supplementation twice daily). At enrolment, after 3- and 6-month supplementation, neurological evaluations (UPDRS III, Hoenh-Yahr scale, l-dopa equivalent dose assessment) were performed and blood sample was collected to define insulin sensitivity (QUICKI index) and oxidative stress (oxidized and reduced glutathione). Repeated measure ANCOVA was applied to define time effect and time × treatment interaction. RESULTS: Participants were comparable at baseline for all assessed parameters. Neurological outcomes and l-dopa requirement were comparable in both group after 6-month of supplementation, without time × treatment interaction. The decrease in insulin sensitivity, as assessed by QUICKI index, observed after 6 months in both groups, was greater in Placebo than in Intervention (time effect p < 0.001; time × treatment interaction p = 0.01). Moreover, despite no changes in total erythrocyte glutathione concentrations, oxidized glutathione levels decreased by 28 ± 17% in the Intervention while increased by 55 ± 38% in Placebo (time effect p = 0.05; time × treatment interaction p = 0.05), after 6-month supplementation. CONCLUSIONS: Amino acid supplementation, assumed with shrewd temporal distribution, did not show detrimental effects on neurological and pharmacological control in protein-restricted Parkinson-affected patients, chronically treated with l-dopa. Furthermore, daily amino acid supplementation partially counteracted insulin resistance development and the loss in antioxidant availability.

Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions.

BACKGROUND AND PURPOSE: The purpose of the present study was to make an attempt to ascertain the etiology of transient global amnesia (TGA), which is still disputed more than 30 years after the first description of this clinical entity. METHODS: In a case-control study, we compared the prevalence of vascular risk factors in 64 TGA patients with 64 first-ever transient ischemic attack (TIA) control subjects and 108 normal community-based control subjects matched for age and sex. We prospectively studied the vascular events and mortality rates of the TGA cases and of the TIA control subjects. Then we compared the outcome of the two groups using actuarial analysis based on survival curves. RESULTS: We did not find evidence of an increased risk of TGA associated with any vascular risk factor. In contrast to TIA control subjects, no TGA patient suffered stroke, myocardial infarction, or TIA during the follow-up period. Migraine was more common in TGA patients than in both normal and TIA control subjects. In three patients (4.5%), the TGA was eventually considered to be of epileptic origin. CONCLUSIONS: The results of our case-control and longitudinal studies point to the conclusion that TGA and TIA do not share the same etiology. Since half of our patients had a precipitating event in their history, it is reasonable to hypothesize that spreading depression may play a role in TGA. The significant positive association between migraine and TGA may support this hypothesis. Epilepsy may mimic TGA in a minority of cases.

Increased density in the middle cerebral artery by nonenhanced computed tomography. Prognostic value in acute cerebral infarction.

In order to consider the prognostic value of hyperdensity of the middle cerebral artery (MCA), we studied retrospectively the medical records of 80 consecutive patients with the diagnosis of ischemic stroke who underwent a non-enhanced computed tomography no longer than 24 h after the onset of the symptoms. To determine the mortality and disability, a follow-up of 30 days was obtained. Mortality does not differ significantly in acute ischemic stroke patients with and without increased density of MCA. When disability, calculated with the Rankin scale, is considered, the two groups are different since patients with hyperdensity of the middle cerebral artery (MCA) have a significantly worse outcome. The two groups do not differ for age, sex, the presence of atrial fibrillation, hypertension, diabetes, myocardial infarction and/or angina, and these factors do not influence the prognosis being equally present in the dead and in the survivors. In the multivariate discriminant analysis with stepwise variable selection, the dense MCA sign was significantly correlated either to mortality or to disability, along with atrial fibrillation, age and diabetes. We conclude that the dense MCA sign can be a useful prognostic factor in the early phase of ischemic stroke.

[Mesoglycan in acute focal cerebral ischemia]. / Il mesoglicano nelle ischemie cerebrali acute a focolaio.

An open, randomized, controlled study including 57 patients with acute cerebral infarct was performed. All the patients, followed and controlled by the same examiner, received, in the first ten days, 24 mg/die i.v. of dexamethasone. 28 patients were also treated with mesoglycan (150 mg/die i.m. for five days and 144 mg/die per os for a further twenty-five days). The differences between the basal and final scores in the mesoglycan group and in the controls were not statistically significant as analysed by the Mann-Whitney U test. The mesoglycan influenced only slightly the laboratory values (PT, PTT, alkaline phosphatase, GOT, GPT, cholesterol and triglycerides, fibrinogen, blood glucose, azotemia and creatinine) performed before the beginning of the treatment, as their changes after thirty days of therapy were in the normal range. The mesoglycan was very well tolerated and no side-effects were observed during the treatment.