Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome in relapsing-remitting multiple sclerosis patients on high-dose interferon ß.

Three women aged 34-47 years old, on high dose interferon beta-1a for relapsing-remitting multiple sclerosis, were hospitalized between 2009-2012 for thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Patients sought medical attention for neurological symptoms including cephalalgia, blurred vision, confusion, focal deficits and seizures. All patients presented thrombocytopenia, hemolytic anemia and arterial hypertension. Despite plasma exchanges, corticosteroids and anti-CD20 treatments, all patients progressed towards severe renal insufficiency and one patient died of hemorrhagic shock. In this report we identify a rare but morbid complication of interferon beta-1a treatment associated with female gender, Caucasian background and low body mass index.

Two routes to losing one's past life: a brain trauma, an emotional trauma.

Organic and psychogenic retrograde amnesia have long been considered as distinct entities and as such, studied separately. However, patterns of neuropsychological impairments in organic and psychogenic amnesia can bear interesting resemblances despite different aetiologies. In this paper, two cases with profound, selective and permanent retrograde amnesia are presented, one of an apparent organic origin and the other with an apparent psychogenic cause. The first case, DD, lost his memory after focal brain injury from a nail gun to the right temporal lobe. The second case, AC, lost her memory in the context of intense psychological suffering. In both cases, pre-morbid autobiographical memory for people, places and events was lost, and no feeling of familiarity was experienced during relearning. In addition, they both lost some semantic knowledge acquired prior to the onset of the amnesia. This contrasts with the preservation of complex motor skills without any awareness of having learned them. Both DD and AC showed mild deficits on memory tests but neither presented any anterograde amnesia. The paradox of these cases--opposite causes yet similar clinical profile--exemplifies the hypothesis that organic and psychogenic amnesia may be two expressions of the same faulty mechanism in the neural circuitry.