[Delirium in old age. Difficulties in diagnosis]. / Syndrome confusionnel du sujet âgé: les difficultés d'un diagnostic facile.

Confusion is a frequent psychiatric and behavioural manifestation of diffuse cerebral injury found in elderly patients that are severely ill or stressed. The hyperactive form is often recognised because of the psychomotor agitation. However, the hypoactive form is most frequent and has a worse prognosis. Despite, it is often under-recognised. Among contributing factors, anticholinergic agents and drug interactions are significant. Identification and treatment of the underlying cause of delirium is essential with a focus on non pharmacological approach. Antipsychotic agents are reserved for severe forms and where non pharmacological intervention fracases.

[Herpes zoster and post-herpetic neuralgia in older adults]. / Zona et névralgies postzostériennes de la personne âgée.

Varicella-Zoster virus is responsible for chickenpox and, after reactivation, herpes zoster. Herpes zoster causes a vesicular dermatomal rash, traditionally metameric. Old adults can present severe pain during the acute phase, and late complications, such as post-herpetic neuralgia that can trying and crippling. Initiated within the first 72 hours of the rash, antivirals accelerate rash healing, reducing both rash and acute pain severity but incompletely the onset of other complications. Complementary therapeutic drug is often necessary. However, their application in old, frail, co-morbid and often poly-medicated patients have to be carefully considered as their use may be contraindicated. A specific vaccine is enable to reduce herpes zoster-related morbidity.

Parkin immunoreactivity in the brain of human and non-human primates: an immunohistochemical analysis in normal conditions and in Parkinsonian syndromes.

The etiology of Parkinson's disease is unknown, but the gene involved in an autosomic recessive form of the disease with early onset has recently been identified. It codes for a protein with an unknown function called parkin. In the present study we produced a specific polyclonal antiserum against human parkin. Immunohistochemical analysis showed that parkin is expressed in neuronal perikarya and processes but also in glial and blood vessels in the primate brain (human and monkey). Electron microscopy indicated that parkin immunoreactivity is mostly located in large cytoplasmic vesicles and at the level of the endoplasmic reticulum. Parkin was expressed heterogeneously in various structures of the brain. It was detectable in the dopaminergic systems at the level of the perikarya in the mesencephalon but also in the striatum. However, parkin was also expressed by numerous nondopaminergic neurons. The staining intensity of parkin was particularly high in the hippocampal formation, the pallidal complex, the red nucleus, and the cerebellum. Comparison of control subjects with patients with Parkinson's disease and control animals with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated animals revealed a loss of parkin-immunoreactive neurons only in the substantia nigra pars compacta. Furthermore, the surviving dopaminergic neurons in the parkinsonian state continued to express parkin at a level similar to that observed in the control situation. These data indicate that parkin is a widely expressed protein. Thus, the degeneration of dopaminergic neurons in familial cases of Parkinson's disease with autosomal recessive transmission cannot be explained solely in terms of an alteration of this protein.