Virus Infections on Prion Diseased Mice Exacerbate Inflammatory Microglial Response.

We investigated possible interaction between an arbovirus infection and the ME7 induced mice prion disease. C57BL/6, females, 6-week-old, were submitted to a bilateral intrahippocampal injection of ME7 prion strain (ME7) or normal brain homogenate (NBH). After injections, animals were organized into two groups: NBH (n = 26) and ME7 (n = 29). At 15th week after injections (wpi), animals were challenged intranasally with a suspension of Piry arbovirus 0.001% or with NBH. Behavioral changes in ME7 animals appeared in burrowing activity at 14 wpi. Hyperactivity on open field test, errors on rod bridge, and time reduction in inverted screen were detected at 15th, 19th, and 20th wpi respectively. Burrowing was more sensitive to earlier hippocampus dysfunction. However, Piry-infection did not significantly affect the already ongoing burrowing decline in the ME7-treated mice. After behavioral tests, brains were processed for IBA1, protease-resistant form of PrP, and Piry virus antigens. Although virus infection in isolation did not change the number of microglia in CA1, virus infection in prion diseased mice (at 17th wpi) induced changes in number and morphology of microglia in a laminar-dependent way. We suggest that virus infection exacerbates microglial inflammatory response to a greater degree in prion-infected mice, and this is not necessarily correlated with hippocampal-dependent behavioral deficits.

PET study and neuropsychological assessment of a long-lasting post-encephalitic parkinsonism.

A 76-year old woman was affected by lethargic encephalitis in 1918, at the age of 3 months. Long-term clinical follow-up with late neuropsychological evaluation revealed post-encephalitic parkinsonism, which worsened very slowly and was improved by levodopa. Obsessive and compulsive disorders (OCD) were associated to nosophobia. Neuropsychological evaluation showed mild visuocontructional memory deficit, which was isolated. 18 Fluoro-Dopa PET demonstrated a severe bilateral and symmetrical reduction in fluoro-dopa uptake, which was more marked in the putamen than in the caudate. Thus, the pattern of dopaminergic denervation was similar to the one observed in idiopathic Parkinson's disease.

[Personality change following encephalitis lethargica in childhood. Eventual fate of a patient]. / Wesensveränderung nach Encephalitis lethargica der Kindheit. Spätschicksal eines Patienten.

An account is given of a patient who died at the age of sixty. He had no recollection of having had encephalitis as a child. In his schooldays, the patient was subject to severe behavioral disorders which were not susceptible to outside influence. During his military service he was frequently punished for conduct prejudicial to discipline and good order, and at the front he was even sentenced to death, but reprieved. His later life brought him no tranquility, ever new conflicts driving him from one job after another. Breaking into uncontrollable fits of rage, he would psychically attack the people around him, threatening to kill them. He was incapable of controlling his impulses. He spent the second half of his life in institutional care, his extrems impulsiveness being the cause of considerable disruption. Post mortem examination confirmed the encephalitis lethargica he was assumed to have suffered as a child, which was responsible for the typical change of character. It is evident how encephalitis lethargica in childhood sets a lifelong mark on the conduct, with appalling consequences.