Spinal accessory neuropathy after deep brain stimulation for Parkinson's disease

We report a man with Parkinson's disease who developed right spinal accessory neuropathy after right subthalamic nucleus deep brain stimulator and infraclavicular pulse generator implantation. He complained of right shoulder pain and weakness in the post-operative period. He was subsequently diagnosed with a right spinal accessory nerve injury, confirmed by neuromuscular electrodiagnostic studies - electromyography (EMG) and nerve conduction (NC) -, possibly caused by a stretch injury to the nerve at the time of creation of the subcutaneous tunnel for placement of the extension lead of the deep brain stimulator system. However, he had near complete clinical resolution of the spinal accessory neuropathy within nine months after surgery. As a result of this complication, we now map the spinal accessory nerve electrophysiologically during deep brain stimulation surgery.     

Human fetal/tumor metakaryotic stem cells: pangenomic homologous pairing and telomeric end-joining of chromatids

Metakaryotic cells and syncytia with large, hollow, bell-shaped nuclei demonstrate symmetrical and asymmetrical amitotic nuclear fissions in microanatomical positions and numbers expected of stem cell lineages in tissues of all three primordial germ layers and their derived tumors. Using fluorescence in situ hybridization, mononuclear metakaryotic interphase cells have been found with only 23 centromeric and 23 telomeric staining regions. Syncytial bell-shaped nuclei found approximately during weeks 5–12 of human gestation display 23 centromeric and either 23 or 46 telomeric staining regions. These images suggest that (1) homologous chromatids pair at centromeres and telomeres, (2) all paired telomeres join end-to-end with other paired telomeres in all mononuclear and some syncytial metakaryotic cells, and (3) telomere junctions may open and close during the syncytial phase of development. Twenty-three telomeric joining figures could be accounted by 23 rings of one chromatid pair each, a single pangenomic ring of 23 joined chromatid pairs, or any of many possible sets of oligo-chromatid pair rings. As telomeric end-joining may affect peri-telomeric gene expression, a programmed sequence of telomeric end-joining associations in metakaryotic stem cells could guide developmental arboration and errors in, or interruptions of, this program could contribute to carcinogenesis.     

Standardizing IV infusion medication concentrations to reduce variability in medication errors

Practical strategies for preventing medication errors in pediatric patients are needed. Medication safety can be improved by assessing current practices, developing evidence-based interventions to improve such practices, evaluating the impact of new evidence-based innovations, and providing feedback to clinicians [20]. Nurses at the point of care are well positioned to identify and implement structures and processes to address medication errors so that the most preventable errors become a thing of the past.     

Presenting research to clinicians: strategies for writing about research findings

Research is of little value to clinical practice if the findings are not appropriately integrated into that practice. While publishing the results of research is essential for translating findings into practice, Marilyn Oermann and colleagues suggest that work is not done until the findings are disseminated for use by clinicians and others who need the research results to guide their practice     

Prefrontal cortex cytoarchitecture in normal aging and Alzheimer’s disease: a relationship with IQ

We have previously shown that the minicolumnar spacing of neurons in the cerebral cortex relates to cognitive ability, and that minicolumn thinning occurs in old age. The present study examines further the relationship between cognitive ability and cortical fine structure (minicolumn organization and neuropathology) in the dorsolateral prefrontal cortex (dlPFC) and the parahippocampal gyrus (PHG) in mild cognitive impairment (MCI) and Alzheimer’s disease (AD). Premortem neuropsychological scores were related to postmortem microanatomy in 58 adults (20 normal controls, 18 MCI, and 20 confirmed AD patients). We found a correspondence between minicolumn thinning in the dlPFC and IQ decline in dementia. In mild impairment, IQ remained stable, as did dlPFC minicolumn width and dlPFC plaque load. IQ only declined as dlPFC minicolumn thinning occurred and dlPFC plaque load increased in more severe dementia. By contrast, plaque load increased and minicolumns became steadily thinner in the PHG, where minicolumn width correlated with declining mini-mental state examination score across both MCI and severe dementia. By including a further 14 younger control subjects, we found that in normal healthy aging, minicolumn width decreased in the dlPFC, whereas PHG minicolumn width did not change. AD patients in our dataset with higher IQ were older at time of death and had less pathology, which supports a neural basis for the cognitive reserve hypothesis.     

Neuronal gap junctions play a role in the secondary neuronal death following controlled cortical impact

Autosomal dominant cerebellar ataxias (ADCAs), genetically classified into spinocerebellar ataxias (SCAs), are a highly heterogeneous group of neurodegenerative disorders. Recently, mutations in the fibroblast growth factor 14 gene (FGF14) have been reported to cause SCA27 subtype. To evaluate the frequency of FGF14 mutations in mainland of China, we performed molecular genetic analysis in 67 unrelated familial ataxia cases and 500 normal controls by denaturing high-performance liquid chromatography (DHPLC) and DNA direct sequencing. Interestingly, we found a pair of siblings carried the same heterozygous variation (c.-10delC) characterized by different clinical features, which is probably a novel insertion/deletion (I/D) polymorphism in the 5'UTR region of the exon 1b. It suggests that SCA27 is a rare subtype in China.