SUMMARY Eight consecutive patients with CT scan evidence of a bilateral infarct in the territory of the paramedian thalamic artery are reported. In seven cases the infarct also extended to the territory of the polar artery. The main symptoms were: (1) disorder of vigilance which cleared in a few days, and hypersomnolence which lasted longer and in two patients was still present a year later; (2) amnesia, detectable clinically in four patients and only with tests in two patients, which persisted in one patient for three years; (3) changes of mood and bulimia present in five and four patients respectively; and (4) vertical gaze paresis in five patients. Only one patient died, and in the remainder the symptoms tended to subside, but none of the patients who could be followed-up for a year returned to normal behaviour. Clinical and CT scan correlations pointed to the mammillo-thalamic tract as the structure whose damage was responsible for the memory disorders.Before computed tomography (CT) infarct of the thalamus was a diagnosis that the clinician could at most suspect, when confronted with a clinical picture resembling the classical Dejerine-Roussy's syndrome,1 but not substantiate in the absence of verification by necropsy. Even more difficult and tentative was the recognition of the other topographical thalamic syndromes that had been reported.2 CT scan has greatly improved our ability to identify in vivo discrete syndromes corresponding to the involvement of the territories supplied by the thalamic arteries. Based on the anatomical description provided by Percheron3 -5 the following types have been identified:6 (1) antero-lateral infarct, associated with polar artery occlusion; (2) postero-lateral infarct, associated with geniculo-thalamic artery occlusion; (3) infero-median infarct, associated with paramedian artery occlusion; and (4) infarct involving the globus pallidus, the posterior limb of the internal capsule and the lateral thalamic nuclei, associated with anterior choroidal artery occlusion.
Foscarnet is a pyrophosphate analogue that has been successfully used in severe cytomegalovirus (CMV) infections. Little is known of the incidence and mechanisms of foscarnet-induced nephrotoxicity as most data comes from recipients of renal allografts or from patients with severe underlying disease or with other nephrotoxic drugs. We have retrospectively analyzed the evolution of renal function after 56 courses of foscarnet. In addition, we have prospectively studied the protective effects of hydration on foscarnet nephrotoxicity (2.5 liters of saline/day during the night before the foscarnet therapy and throughout the course of treatment). Foscarnet-induced acute renal failure was defined as a rise in serum creatinine of at least 25% from the basal value. An increase in serum creatinine occurred in 37 cases out of the 56 courses of foscarnet (66%). The mean serum creatinine prior to foscarnet was 80.5 ± 3.3 μmol/l and the mean increase was 190 ± 28.3 μmol/l (range 80–1,000). Peak serum creatinine was higher than 200 and 300 μmol/l in 16 and 13 patients, respectively. Kidney obtained at autopsy from a 30-year-old male with AIDS, CMV pneumonitis and acute renal failure secondary to foscarnet administration showed an extensive tubular necrosis. In the group which was prospectively hydrated only 1 patient had an acute renal failure. The mean serum creatinine at the peak (96 ± 4 μmol/l) and at the end of the treatment (83 ± 4 μmol/l) was significantly lower (p < 0.05) than in non hydrated patients. In conclusion, foscarnet is a highly nephrotoxic drug which induces acute tubular necrosis. Prehydration with 2.5 liters of isotonic saline throughout the course of foscarnet therapy almost completely abolishes its nephrotoxicity.
Shiga toxin-producing Escherichia coli (STEC), responsible for the hemolytic uremic syndrome, is an endemic pathogen in Argentina. We studied the prevalence of STEC in fecal samples from cats and dogs of Buenos Aires city and suburbs. Cultures were used for screening stx1/stx2 and rfbO157 by multiplex PCR. All E. coli-positive colonies for these genes were further characterized for the eae gene and for serotypes. In dogs, 17 (3.7%), 19 (4.2%) and 34 (7.5%) of samples were positive for stx2, stx1 and rfb, respectively. In cats, six (4.0%) of the samples were positive for stx2, three (2.0%) for stx1 and four (2.7%) for rfbO157. In 18 (4.0%) of the dog samples, a bacteriological diagnosis was obtained by isolation. The percentage of positive isolates corresponding to the rfbO157 and to the stx2 genotypes were 2.9% and 1.1%, respectively. In four of the cat samples, the bacteriological diagnosis for stx2 (2.6% prevalence of STEC) was confirmed. Although these data suggest that the high infection index of STEC in children in Argentina does not seem to be due mainly to the role of cats and dogs, there are some strains with virulence genes in common for humans and their domestic animals.
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