Brain muscarinic cholinergic receptors in Huntington's disease

Muscarinic cholinergic receptors and choline acetyltransferase (ChAT) activity were studied in postmortem brain tissue from patients with Huntington's disease and matched control subjects. In comparison with controls, reductions in ChAT activity were found in the hippocampus, but not in the temporal cortex in Huntington's disease. Patients with Huntington's disease showed reduced densities of the total number of muscarinic receptors and of M-2 receptors in the hippocampus while the density of M-1 receptors was unaltered. Muscarinic receptor binding was unchanged in the temporal cortex. These results indicate a degeneration in Huntington's disease of the septo-hippocampal cholinergic pathway, but no impairment of the innominato-cortical cholinergic system

Diagnostic precision of image-guided multisampling core needle biopsy of suspected lymphomas in a primary care hospital

We evaluated the diagnostic quality of image-guided multisampling core needle biopsy (CNB) in patients investigated for suspected lymphoma in a primary care hospital. A total of 112 patients were consecutively assessed during a 3-year period. There were 80 lymphoid site biopsies and 32 non-lymphoid site biopsies. Eight to nine cores were obtained from different parts of the biopsy site. Two cores were systematically frozen, allowing for further morphological, immunochemistry and molecular studies. The diagnostic yield of CNB for malignancy was 100%. Only 47% (41/87) of patients with initial suspicion of lymphoma were finally diagnosed with Lymphoma. The diagnostic yield of CNB for lymphoma typing was 98% (62/63), according to the WHO classification. The diagnostic yield of CNB for complete lymphoma subtyping/grading was 86% (54/63). The diagnostic yield of CNB for a definite diagnosis of benignity was only 47% (8/17). In a primary care setting, multisampling CNB is a minimally invasive, and very accurate procedure for confirming malignancy in patients with suspected lymphoma, presenting with superficial/deep-seated, lymphoid/non-lymphoid site targets. With a very high diagnostic yield for lymphoma typing and a high diagnostic yield for complete lymphoma subtyping/grading a therapeutic decision can be taken in most patients

New Therapies, Old Problems, or, A Plea for Neuromodesty

This article suggests that investigation deep brain stimulation (DBS) for mental disorders raises few new bioethical issues. Although the scientific basis of the procedure may be both complex and largely unknown, addressing informed consent in such situations is a familiar problem. After reviewing the legal and moral background for investigating DBS and the scientific difficulties DBS faces as a potential treatment for mental disorders, the articles focuses on informed consent and makes two primary suggestions. The study of DBS may proceed, but hyper-disclosure of the complexities should be required for competent subjects or proper surrogates if the candidate is not competent, and the most rigorous standard for competence should be employed. Throughout, neuromodesty and caution are urged

Goal-directed and habitual control in the basal ganglia: implications for Parkinson's disease

Progressive loss of the ascending dopaminergic projection in the basal ganglia is a fundamental pathological feature of Parkinson's disease. Studies in animals and humans have identified spatially segregated functional territories in the basal ganglia for the control of goal-directed and habitual actions. In patients with Parkinson's disease the loss of dopamine is predominantly in the posterior putamen, a region of the basal ganglia associated with the control of habitual behaviour. These patients may therefore be forced into a progressive reliance on the goal-directed mode of action control that is mediated by comparatively preserved processing in the rostromedial striatum. Thus, many of their behavioural difficulties may reflect a loss of normal automatic control owing to distorting output signals from habitual control circuits, which impede the expression of goal-directed action

Microsurgery can cure most intracranial dural arteriovenous fistulae of the sinus and non-sinus type

There is consensus that intracranial dural arteriovenous fistulae (dAVF) with direct (non-sinus-type) or indirect (sinus-type) retrograde filling of a leptomeningeal vein should be treated due to the high risk of neurological deficits and hemorrhage. No consensus exists on treatment modality (surgery and/or embolization) and, if surgery is performed, on the best surgical strategy. This series aims to evaluate the role of surgery in the management of aggressive dAVFs. Forty-two patients underwent surgery. Opening and packing the sinus with thrombogenic material was performed in 9 of the 12 sinus-type dAVFs. In two sinus-type fistulae of the cavernous sinus and 1 of the torcular, microsurgery was used as prerequisite for subsequent embolization by providing access to the sinus. In the 30 non-sinus-type dAVFs, surgery consisted of interruption of the draining vein at the intradural entry point. In 41 patients undergoing 43 operations, elimination of the dAVF was achieved (97.6%). In one case, a minimal venous drainage persisted after surgery. The transient surgical morbidity was 11.9% (n = 5) and the permanent surgical morbidity 7.1% (n = 3). Our surgical strategy was to focus on the arterialized leptomeningeal vein in the non-sinus-type and on the arterialized sinus segment in the sinus-type dAVFs allowing us to obliterate all but one dAVF with a low morbidity rate. We therefore propose that microsurgery should be considered early in the treatment of both types of aggressive dAVFs. In selected cases of cavernous sinus dAVFs, the role of microsurgery is reduced to that of an adjunct to endovascular therapy

Attentional Set-Shifting Deficit in Parkinson’s Disease Is Associated with Prefrontal Dysfunction: An FDG-PET Study

The attentional set-shifting deficit that has been observed in Parkinson’s disease (PD) has long been considered neuropsychological evidence of the involvement of meso-prefrontal and prefrontal-striatal circuits in cognitive flexibility. However, recent studies have suggested that non-dopaminergic, posterior cortical pathologies may also contribute to this deficit. Although several neuroimaging studies have addressed this issue, the results of these studies were confounded by the use of tasks that required other cognitive processes in addition to set-shifting, such as rule learning and working memory. In this study, we attempted to identify the neural correlates of the attentional set-shifting deficit in PD using a compound letter task and 18F-fluoro-deoxy-glucose (FDG) positron emission tomography during rest. Shift cost, which is a measure of attentional set-shifting ability, was significantly correlated with hypometabolism in the right dorsolateral prefrontal cortex, including the putative human frontal eye field. Our results provide direct evidence that dysfunction in the dorsolateral prefrontal cortex makes a primary contribution to the attentional set-shifting deficit that has been observed in PD patients