The use of implants that can electrically stimulate or record electrophysiological or neurochemical activity in nervous tissue is rapidly expanding. Despite remarkable results in clinical studies and increasing market approvals, the mechanisms underlying the therapeutic effects of neuroprosthetic and neuromodulation devices, as well as their side effects and reasons for their failure, remain poorly understood. A major assumption has been that the signal-generating neurons are the only important target cells of neural-interface technologies. However, recent evidence indicates that the supporting glial cells remodel the structure and function of neuronal networks and are an effector of stimulation-based therapy. Here, we reframe the traditional view of glia as a passive barrier, and discuss their role as an active determinant of the outcomes of device implantation. We also discuss the implications that this has on the development of bioelectronic medical devices.

/pdf/glial-responses-to-implanted-electrodes-in-the-brain-50jku1y6dp.pdf

Glial responses to implanted electrodes in the brain.

Neurofibrillary tangles (NFT) and neurites associated with senile plaques (SP) in Alzheimer disease-affected brain tissues were specifically immunostained with affinity-purified antibody preparations directed against ubiquitin. In addition, a class of neurites seen in brain regions containing NFT and SP were also specifically stained. Cross-reactivity of the ubiquitin antisera for tau protein, neurofilament proteins, and high molecular weight microtubule-associated proteins (MAPs) were ruled out by (i) the inability of the ubiquitin antisera to stain these proteins in immunoblotting experiments and (ii) the inability of tau, neurofilament, and MAP preparations, when preincubated with the ubiquitin antisera, to inhibit the selective neurofibrillar staining observed. Our results are consistent with the suggestion that ubiquitin is covalently associated with the insoluble neurofibrillary material of NFT and SP. We propose that the ubiquitin-mediated degradative pathway may be ineffective in removing these fibrillar structures in Alzheimer disease brain.

Ubiquitin is detected in neurofibrillary tangles and senile plaque neurites of Alzheimer disease brains

Background:

We report on a double-blind, crossover pilot trial for the treatment of rapid eye movement behavior disorder (RBD) in 12 patients with Parkinson's disease in whom conventional therapy failed.



Methods:

We employed a patch of the cholinesterase inhibitor rivastigmine at a dose of 4.6 mg/24 hours for 3 weeks compared with placebo to reduce the frequency of RBD episodes. The number of RBD episodes was monitored by diaries of bed partners.



Results:

Rivastigmine was well tolerated in most patients, with minor side effects, mainly related to peripheral cholinergic action, and significantly reduced the mean frequency of RBD episodes during the observation time.



Conclusions:

The results of this pilot trial need to be confirmed by further studies on a larger number of patients. © 2012 Movement Disorder Society

Rivastigmine as alternative treatment for refractory REM behavior disorder in Parkinson's disease.

Objective
Deep brain stimulation (DBS) is an effective therapy for the treatment of a number of movement and neuropsychiatric disorders. The effectiveness of DBS is dependent on the density and location of stimulation in a given brain area. Adjustments are made to optimize clinical benefits and minimize side effects. Until recently, clinicians would adjust DBS settings using a voltage mode, where the delivered voltage remained constant. More recently, a constant-current mode has become available where the programmer sets the current and the stimulator automatically adjusts the voltage as impedance changes.

Methods
We held an expert consensus meeting to evaluate the current state of the literature and field on constant-current mode versus voltage mode in clinical brain-related applications.

Results/Conclusions
There has been little reporting of the use of constant-current DBS devices in movement and neuropsychiatric disorders. However, as impedance varies considerably between patients and over time, it makes sense that all new devices will likely use constant current.

The rationale driving the evolution of deep brain stimulation to constant-current devices.

The diagnosis of psychogenic movement disorders (PMDs) may be challenging, given the lack of accurate and reliable tests.1 Two sets of clinical criteria, the Fahn-Williams (FW)2 and Shill-Gerber (SG)3 criteria, have been developed to assist in the diagnostic process and avoid the diagnosis-by-exclusion approach to PMD. Reliability and applicability of these criteria are essential because misdiagnosis may delay the initiation of appropriate treatment, leading to poor outcomes.4

We measured interobserver diagnostic agreement and clinical certainty judgment (according to FW and SG criteria) of PMD among movement disorder specialists (MDS) and general neurologists (non-MDS). We also examined whether diagnostic agreement based exclusively on motor phenomenology was satisfactory.

/pdf/diagnostic-agreement-in-patients-with-psychogenic-movement-160lat11kz.pdf

Diagnostic Agreement in Patients With Psychogenic Movement Disorders

Over 70,000 DBS devices have been implanted worldwide; however, there remains a paucity of well-characterized post-mortem DBS brains available to researchers. We propose that the overall understanding of DBS can be improved through the establishment of a Deep Brain Stimulation-Brain Tissue Network (DBS-BTN), which will further our understanding of DBS and brain function. The objectives of the tissue bank are twofold: (a) to provide a complete (clinical, imaging and pathological) database for DBS brain tissue samples, and (b) to make available DBS tissue samples to researchers, which will help our understanding of disease and underlying brain circuitry. Standard operating procedures for processing DBS brains were developed as part of the pilot project. Complete data files were created for individual patients and included demographic information, clinical information, imaging data, pathology, and DBS lead locations/settings. 19 DBS brains were collected from 11 geographically dispersed centers from across the U.S. The average age at the time of death was 69.3 years (51–92, with a standard deviation or SD of 10.13). The male:female ratio was almost 3:1. Average post-mortem interval from death to brain collection was 10.6 h (SD of 7.17). The DBS targets included: subthalamic nucleus, globus pallidus interna, and ventralis intermedius nucleus of the thalamus. In 16.7% of cases the clinical diagnosis failed to match the pathological diagnosis. We provide neuropathological findings from the cohort, and perilead responses to DBS. One of the most important observations made in this pilot study was the missing data, which was approximately 25% of all available data fields. Preliminary results demonstrated the feasibility and utility of creating a National DBS-BTN resource for the scientific community. We plan to improve our techniques to remedy omitted clinical/research data, and expand the Network to include a larger donor pool. We will enhance sample preparation to facilitate advanced molecular studies and progenitor cell retrieval.

The national DBS brain tissue network pilot study: need for more tissue and more standardization

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The national DBS brain tissue network pilot study: need for more tissue and more standardization