Spread Deficits in Initiation, Speed and Accuracy of Horizontal and Vertical Automatic Saccades in Dementia with Lewy Bodies

Background: Mosimann et al. (2005) reported prolongation of saccade latency of prosaccades in dementia with Lewy body (DLB). The goal of this study is to go further examining all parameters, such as rates of express latency, but also accuracy and velocity of saccades, and their variability. Methods: We examined horizontal and vertical saccades in 10 healthy elderly subjects and 10 patients with DLB. Two tasks were used: the gap (fixation target extinguishes prior to target onset) and the overlap (fixation stays on after target onset). Eye movements were recorded with the Eyelink II eye tracker. Results: The main findings were: (1) as for healthy, latencies were shorter in the gap than in the overlap task (a gap effect); (2) for both tasks latency of saccades was longer for DLB patients and for all directions; (3) express latency in the gap task was absent for large majority of DLB patients while such saccades occurred frequency for controls; (4) accuracy and peak velocity were lower in DLB patients; (5) variability of all parameters was abnormally high in DLB patients. Conclusions: Abnormalities of all parameters, latency, accuracy and peak velocity reflect spread deficits in cortical-subcortical circuits involved in the triggering and execution of saccades

Etude clinocopathologique prospective de dix-huit patients présentant une maladie à corps de Lewy

PARIS6-Bibl.Pitié-Salpêtrie (751132101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Apport du raisonnement gériatrique dans la prise en charge d'une crise épileptique ou d'une épilepsie

International audienceEpileptic seizures and epilepsy appear frequent in the elderly. The diagnosis is often more difficult and therapeutic decisions are often debated. In this context, the implementation of a rigorous analysis and reasoning to correctly determine the various components at the origin of the epileptic seizure is fundamental. Some data are in favor of a decrease of the epileptogenic threshold with advancing age. But, this is in no way sufficient to account for the occurrence of a seizure. It is necessary to add to aging factor a chronic pathology responsible for brain lesions (micro or macroscopic: stroke, Alzheimer's disease, brain tumors...) and/or acute aggression (trauma, central nervous system infection, metabolic or toxic disorders...) to trigger a seizure. It is notable that an association of some mild brain lesions and a weak metabolic disturbance could trigger a seizure. In these cases, the probability of trigger a new seizure with another mild precipitant factor appears very high. This analysis is necessary and particularly useful in these multi-pathological patients. It also makes it easier to decide whether to start antiepileptic treatment. In case of a triggering factor such as hyponatremia, for example, in the absence of associated underlying lesions, it seems legitimate not to start treatment at the first epileptic seizure. On the other hand, if hyponatremia (often less deep than in the previous case) is associated with sequel of stroke or Alzheimer's disease, it seems reasonable to start treatment quickly.Les crises d’épilepsie et l’épilepsie sont fréquentes dans la population gériatrique. Le diagnostic est souvent plus difficile et les prises de décisions thérapeutiques plus délicates. Dans ce contexte, un raisonnement rigoureux permettant de déterminer les différents facteurs à l’origine de la crise est fondamental chez ces patients multipathologiques. Si l’on peut admettre que le seuil épileptogène diminue avec l’âge, cela n’est en rien suffisant pour rendre compte de la survenue d’une crise. Il faut, à ce facteur de vieillissement, ajouter une pathologie chronique responsable de lésions cérébrales micro- ou macroscopiques (accident vasculaire cérébral (AVC), maladie d’Alzheimer, tumeur cérébrale…) et/ou une agression aiguë (traumatisme, infection du système nerveux central, troubles métaboliques, toxiques…). Le raisonnement gériatrique prend en compte l’intrication de plusieurs facteurs, souvent insuffisants en eux-mêmes pour déclencher une crise. Il permet également de faciliter la décision de débuter ou non un traitement antiépileptique. En cas de facteur déclenchant comme une hyponatrémie par exemple, en l’absence de lésion cérébrale associée, il paraît légitime de ne pas débuter de traitement à la première crise. En revanche, si l’hyponatrémie (souvent moins profonde que dans le cas précédent) survient chez un patient dit « cérébro-lésé », il paraît raisonnable de débuter un traitement rapidement

An Unusual Case of Hemiballism-Hemichorea Associated with Nonketotic Hyperglycemia in Association with a Centrum Semiovale Stroke

International audienceWe report a case of hemiballism-hemichorea associated with nonketotic hyperglycemia, in a patient with a centrum semiovale strok

Klebsiella pneumoniae necrotizing fasciitis of the leg in an elderly French woman

International audienceKlebsiella pneumoniae necrotizing fasciitis is a rare infection in regions outside of Asia. Here, we present a case of necrotizing fasciitis of the leg caused by K. pneumoniae in a 92-year-old French woman hospitalized in a geriatric rehabilitation unit. The patient initially presented with dermohypodermitis of the leg that developed from a dirty wound following a fall. A few hours later, this painful injury extended to the entire lower limb, with purplish discoloration of the skin, bullae, and necrosis. Septic shock rapidly appeared and the patient died 9 hours after the onset of symptoms. The patient was Caucasian, with no history of travel to Asia or any underlying disease. Computed tomography revealed no infectious metastatic loci. Blood cultures showed growth of capsular serotype K2 K. pneumoniae strains with virulence factors RmpA, yersiniabactin and aerobactin. This rare and fatal case of necrotizing fasciitis caused by a virulent strain of K. pneumoniae occurred in a hospitalized elderly woman without risk factors. Clinicians and geriatricians in particular should be aware of this important albeit unusual differential diagnosis

LATE-ONSET BING-NEEL SYNDROME ASSOCIATED WITH DELIRIUM AND LEWY BODY DEMENTIA

International audienceno abstrac

Link between non hypoxemic chronic obstructive pulmonary disease and executive functioning in oldest old

International audienceBackground. COPD (chronic obstructive pulmonary disease) may result in cognitive disorders (mainly executive) even without hypoxemia. Methods. The aim of this descriptive study was to highlight a deficit in task-switching in non-hypoxemic patient with COPD and mild cognitive impairment (MCI) or Alzheimer disease (AD). The main judgment criterion was patients' performances on the TMTA and B. COPD patients were recruited via the database (CogDisCo) of the geriatric medicine department at Pitie Salpetriere hospital in Paris. Results. 7 patients had Alzheimer's disease (AD), and 11 mild cognitive impairment (MCI): they were matched for age, sex, MMSE, education level with controls subjects without COPD. There was no significant difference between the two groups. However, patients with COPD and MCI required, on average, an extra 13 seconds compared with patient without COPD for the TMTA and 18 seconds for the TMTB. Patients with COPD and AD needed, on average, an extra 63 seconds for TMTA and 97 seconds for TMTB. The number of errors for the TMTB was the same in the both groups. Conclusion. This preliminary study does not show statistically significant results but the time for achieving TMT was longer in the population with COPD whether AD or MCI. These results encourage us to continue with prospective studies on larger samples

Research in motion: the enigma of Parkinson's disease pathology spread

Neuropathological changes in Parkinson's disease progress slowly and spread according to a characteristic pattern. Recent papers have shed light on this progression of pathology by examining the fate of neurons grafted into the brains of patients with Parkinson's disease. Two of these studies demonstrate that grafted healthy neurons can gradually develop the same pathology as host neurons in the diseased brains. According to these studies, implanted neurons developed alpha-synuclein- and ubiquitin-positive Lewy bodies more than a decade after transplantation. We discuss the possible underlying mechanisms and their implications for how pathology spreads in Parkinson's disease