“When are we going to move?”

Recent reports have indicated that many rehousing projects, moving people out of hospitals large and small, suffer periods of delay. This article relates the frustrations and delays experienced by one such project and, in particular, the effects on five people who were the first due to move into a home of their own within the project. The article argues that staff working on such schemes should acknowledge that such delays are very likely and do all they can to minimise the effects on the residents involved.     

Who was the man who discovered the “Lewy bodies”?

In 1912, Fritz Heinrich Lewy described neuronal inclusions in the brain of patients who had suffered from Paralysis agitans (i.e., Parkinson's disease). Later, these findings became the so‐called “Lewy bodies.” However, little is known about the man who made this discovery. Our aim was to investigate Lewy's private and professional life and to gather information for a detailed biography. We contacted over 100 archives, libraries, and museums in Germany, Poland, Switzerland, United Kingdom, and United States. Over 300 documents, publications, and photos were collected. Lewy was born in Berlin, Germany in 1885 and lived there until 1933. After his dismissal on racial grounds by the Nazis, Lewy emigrated to England in 1933 and to the United States of America in 1934, where he lived and worked until his death in 1950. This article gives a summary of Lewy's life and briefly presents his contribution to German and American neurology. © 2010 Movement Disorder Society     

Where is the “where” in the brain? A meta‐analysis of neuroimaging studies on spatial cognition

Spatial representations are processed in the service of several different cognitive functions. The present study capitalizes on the Activation Likelihood Estimation (ALE) method of meta‐analysis to identify: (a) the shared neural activations among spatial functions to reveal the “core” network of spatial processing; (b) the specific neural activations associated with each of these functions. Following PRISMA guidelines, a total of 133 fMRI and PET studies were included in the meta‐analysis. The overall analysis showed that the core network of spatial processing comprises regions that are symmetrically distributed on both hemispheres and that include dorsal frontoparietal regions, presupplementary motor area, anterior insula, and frontal operculum. The specific analyses revealed the brain regions that are selectively recruited for each spatial function, such as the right temporoparietal junction for shift of spatial attention, the right parahippocampal gyrus, and the retrosplenial cortex for navigation and spatial long‐term memory. The findings are integrated within a systematic review of the neuroimaging literature and a new neurocognitive model of spatial cognition is proposed.     

Is “subcortical dementia” a recognizable clinical entity?

The concept of "subcortical dementia" is controversial, lacking clinical validation and having only a questionable pathological basis. Over 100 patients with Alzheimer's, Parkinson's or Huntington's disease, subdivided into three functional disability stages, were given a brief quantitative neuropsychological assessment. Patients with Huntington's or Parkinson's disease were less intellectually impaired than those with Alzheimer's disease at each functional stage. Criteria for dementia were present in all of the Alzheimer's patients but in only half of the Huntington's and Parkinson's disease groups. Patients with similar overall intellectual function scores had no distinct pattern of neuropsychological test performance. Depression, absent in patients with Alzheimer's disease, was present in half the patients with Huntington's and Parkinson's disease and was correlated with intellectual decline. The concept of subcortical dementia is misleading. The pattern of neuropsychological impairment is not distinct, and the neuropathological basis of dementia in these diseases may result from a combination of cortical and subcortical degeneration.     

Are the yips a task‐specific dystonia or “golfer's cramp”?

This study compared golfers with and without the yips using joint movement and surface electromyographic detectors. Fifty golfers (25 with and 25 without complaints of the yips) were studied while putting. All putts were videotaped. Surface electromyography assessed arm cocontraction. A CyberGlove II (Immersion Technologies, Palo Alto, CA) assessed right‐arm angular movements. Primary analysis was done by subjective complaint of the yips, whereas secondary analysis was done by video evidence of an involuntary movement. When grouped by subjective complaints, there were no differences in any movement parameter. When grouped by video evidence of an involuntary movement, yips cases had more (P < 0.001) angular movement in wrist pronation/supination and a trend (P = 0.08) for wrist flexor/extensor cocontraction (yips: 7 of 17, 41.2%; no yips: 6 of 33, 18.2%). Golfers with video evidence of an involuntary movement while putting have excessive rotation of the right wrist in a pronation/supination motion and, as previously reported, a trend for wrist flexor/extensor cocontraction. © 2011 Movement Disorder Society     

Do Reactive Post‐Resection “Injury” Spikes Exist?

PURPOSE: New post-resection spikes on electrocorticography (ECoG) after lesionectomy in patients with seizures may represent residual epileptogenic tissue or presumed reactive injury spikes. We investigated the existence of post-resection injury spikes by eliminating the possibility of residual epileptogenic tissue. METHODS: Preresection and post-resection ECoG was performed on seven patients with an intra-axial neocortical tumor (glioblastoma multiforme or metastasis) and no history of seizures. All tumors were gross-totally resected. RESULTS: The mean age of the patients was 59 years. The tumor location was frontal in four patients, parietal in two, and temporal in one. Two patients had preresection spikes with an average rate of 68 spikes/min that disappeared after surgery. Two different patients had new post-resection spikes, with an average firing rate of 4 spikes/min, despite normal preresection ECoG. In one of these patients, the new spikes were superimposed over a burst suppression pattern. Neither patient developed seizures after surgery. CONCLUSIONS: Surgical irritation of the neocortex is sufficient to produce reactive post-resection epileptogenic discharges surrounding an intra-axial neocortical tumor even in the absence of preoperative seizures and spikes. Injury spikes fire at a slow rate and are not predictive of clinical seizures.