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.     

“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.     

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.     

The mirror‐neuron system and handedness: A “right” world?

To assess the relationship between the mirror-neuron system (MNS), an observation-execution matching system, and handedness, we acquired functional magnetic resonance imaging from 11 right-handed (RH) and eight left-handed (LH) subjects to identify regions involved in processing action (execution and observation) of the right and left upper limbs. During the execution tasks, LH subjects had a more bilateral pattern of activation than RH. An interaction between handedness and hand observed during the observation conditions was detected in several areas of the MNS and the motor system. The within- and between-groups analyses confirmed different lateralizations of the MNS and motor system activations in RH and LH subjects during the observation tasks of the dominant and nondominant limbs. The comparison of the execution vs. observation task demonstrated that during the execution task with their dominant limbs, RH subjects activated areas of the motor system in the left hemisphere, whereas LH subjects also activated areas of the MNS. During the execution task with the nondominant limbs, both groups activated regions of the MNS and motor system. Albeit this study is based on a small sample, the patterns of MNS activations observed in RH and LH subjects support the theory that suggests that this system is involved in brain functions lateralization. In LH people, this system might contribute to their adaptation to a world essentially built for right-handers through a mechanism of mirroring and imitation.     

Dystrophin or a “related protein” in Duchenne muscular dystrophy?

Previously we have shown low levels of dystrophin immunoreactivity in muscle from patients with DMD. According to the "frame-shift hypothesis" DMD muscle should not synthesize any dystrophin through to the C-terminus and it has been suggested that the protein detected is not dystrophin, but a related autosomal homologue. We have labelled serial sections of DMD muscle with specific monoclonal antibodies to the amino, rod and C-terminal domains of dystrophin and find labelling on the same individual fibres, allowing us to conclude that the protein detected is Xp21-encoded dystrophin. This has an impact on the interpretation of myoblast transfer experiments. The abundance (on blots) of "C-terminal dystrophin" appears lower than "rod dystrophin" in both BMD and DMD.     

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     

The thymus in myasthenia gravis: Site of “innate autoimmunity”?

Myasthenia gravis (MG) is an autoimmune disorder caused, in most cases, by autoantibodies against components of the neuromuscular junction, frequently the acetylcholine receptor (AChR), and less often the muscle-specific kinase receptor. The thymus plays a major role in the pathogenesis of MG with anti-AChR antibodies: it shows marked pathologic alterations (hyperplastic or tumoral) in most AChR-positive patients and contains the elements required to initiate and sustain an autoimmune reaction (AChR autoantigen, AChR-specific T cells, and autoantibody-secreting plasma cells). In this study we review early and more recent findings implicating the thymus as site of AChR autosensitization in MG and briefly discuss the therapeutic role of thymectomy. We also summarize data showing that the MG thymus is in a state of chronic inflammation, and we review emerging evidence of a viral contribution to the onset and maintenance of the thymic autoimmune response.     

Neuropsychology of epilepsy in old age – English Version

Clinical Epileptology - Infolge des demografischen Wandels nimmt die Häufigkeit von Epilepsien im höheren Alter zu. Zudem wird ein Zusammenhang von Epilepsien und einem beschleunigten...     

Can “functional” constipation be considered as a form of enteric neuro‐gliopathy?

Constipation has been traditionally viewed and classified as a functional or idiopathic disorder. However, evidence has been accumulating that suggests how constipation might be considered as due to abnormalities of the enteric nervous system, since alterations of this system, not evident in conventional histological examination, may be present in these patients. These abnormalities often consist in decrease or loss of the enteric glial cells, a pathological finding present in most types of constipation so far investigated. In this article we will discuss these evidences, and will try to consider constipation no more as a simple functional or idiopathic disorder but as a form of enteric neuro-gliopathy.