Comparison of treatment modalities in burning mouth syndrome

Background: Burning mouth syndrome (BMS) is characterized by a spontaneous burning pain in the oral mucosa without known organic cause or standardized treatment. The aims of this study were to assess and compare the efficacy of clonazepam and diazepam in relieving the symptoms associated with BMS and evaluate for which patients this treatment might be effective by correlating treatment efficacy with underlying psychological status. Methods: The medical records of BMS patients attending an oral medicine private practice (1999–2004) were reviewed. The patients were then contacted and asked to complete a short questionnaire regarding their response to diazepam/clonazepam drug therapies. A second group of patients attending the above clinic (n = 30) were asked to fill out a hospital anxiety and depression assessment form in an attempt to correlate treatment success with underlying psychological status. Results: A total of 71.4 per cent of patients treated with clonazepam had partial or complete resolution of their oral symptoms, while 55.1 per cent of patients treated with diazepam had improvement of their oral symptoms. There was no correlation between underlying anxiety or depression and efficacy of benzodiazepine medication. Conclusions: A greater percentage of patients taking clonazepam reported either partial or complete relief of symptoms compared to diazepam. However, the differences were not statistically significant. There was no correlation found between underlying psychopathology and treatment success with benzodiazepines.     

Mice lacking alpha-synuclein are resistant to mitochondrial toxins

Abnormalities in the function of alpha-synuclein are implicated in the pathogenesis of Parkinson's disease (PD). We found that alpha-synuclein-deficient mice are resistant to MPTP-induced degeneration of dopaminergic neurons. There was dose-dependent protection against loss of both dopamine in the striatum and dopamine transporter (DAT) immunoreactive neurons in the substantia nigra. These effects were not due to alterations in MPTP processing. We found that alpha-synuclein-deficient mice are also resistant to both malonate and 3-nitropropionic acid (3-NP) neurotoxicity. There was reduced generation of reactive oxygen species in alpha-synuclein-deficient mice following administration of 3-NP. These findings implicate alpha-synuclein as a modulator of oxidative damage, which has been implicated in neuronal death produced by MPTP and other mitochondrial toxins.     

Neuropathologic, neurochemical and immunocytochemical characteristics of aluminum-induced neurofilamentous degeneration

Inoculation of aluminum salts or metallic aluminum into the central nervous system of rabbits produces an encephalomyelopathy accompanied by widespread neurofibrillary degeneration (NFD) affecting restricted neuronal populations. Some investigators have suggested that this preparation may serve as an animal model for human neurodegenerative disorders, such as Alzheimer's disease (AD), in which neurofibrillary tangle (NFT) formation is a prominent histopathologic finding. However, neurochemical, immunocytochemical and behavioral features of the model are largely unknown and its neuropathology only partially described. We have undertaken a series of experiments designed to further characterize these aspects of the model. We have used an intraventricular route of injection of aluminum chloride and found that the distribution of NFD in rabbit brain is similar to the distribution of NFT formation in AD. Immunocytochemical probes demonstrate that phosphorylated neurofilaments accumulate in neuronal perikarya containing NFD, and double labelling techniques suggest that NFD affects primarily projection type neurons. The neurochemical profile of aluminum intoxicated rabbits shows both similarities and discrepancies to that of AD. Finally, as reported in a companion article in this issue of Neurotoxicology (Solomon and Pendlebury, 1988), aluminum-exposed rabbits develop learning and memory deficits which are strongly correlated with the degree of whole brain NFD but not with motor, sensory or motivational factors. We conclude that aluminum-induced NFD may have relevance for understanding NFT formation in AD and other neurodegenerative disorders in which abnormalities of the neuronal cytoskeletal architecture are present.     

HbA1c �C ein Allesk?nner?

The HbA1c value is an important clinical parameter for assessment of the accuracy of the diabetes adjustment and the development or progression of secondary complications of diabetes. An essential condition for such a criterion is high measurement accuracy. Therefore some comments on the accuracy of measurement of glucose and HbA1c values are made at the beginning of this article. Particular emphasis is placed on the fact that despite standardization of HbA1c measurement there are a number of indications where the long-term average glucose level will be overestimated or underestimated by HbA1c_. Some information will be given on the question to what extent usable values for the average glucose level can be estimated from HbA1c followed by some epidemiological findings in particular on the dependence of the prevalence of diabetes on the diagnosis criterion selected. With respect to a number of open questions an algorithm proposed by the German Diabetes Society (DDG) is recommended which integrates both diagnostic criteria.     

VA’s National PTSD Brain Bank: a National Resource for Research

The National PTSD Brain Bank (NPBB) is a brain tissue biorepository established to support research on the causes, progression, and treatment of PTSD. It is a six-part consortium led by VA’s National Center for PTSD with participating sites at VA medical centers in Boston, MA; Durham, NC; Miami, FL; West Haven, CT; and White River Junction, VT along with the Uniformed Services University of Health Sciences. It is also well integrated with VA’s Boston-based brain banks that focus on Alzheimer’s disease, ALS, chronic traumatic encephalopathy, and other neurological disorders. This article describes the organization and operations of NPBB with specific attention to: tissue acquisition, tissue processing, diagnostic assessment, maintenance of a confidential data biorepository, adherence to ethical standards, governance, accomplishments to date, and future challenges. Established in 2014, NPBB has already acquired and distributed brain tissue to support research on how PTSD affects brain structure and function.     

Mice lacking cytosolic copper/zinc superoxide dismutase display a distinctive motor axonopathy.

OBJECTIVE: To characterize the motor neuron dysfunction in two models by performing physiologic and morphometric studies. BACKGROUND: Mutations in the gene encoding cytosolic superoxide dismutase 1 (SOD1) account for 25% of familial ALS (FALS). Transgenes with these mutations produce a pattern of lower motor neuron degeneration similar to that seen in patients with FALS. In contrast, mice lacking SOD1 develop subtle motor symptoms by approximately 6 months of age. METHODS: Physiologic measurements, including motor conduction and motor unit estimation, were analyzed in normal mice, mice bearing the human transgene for FALS (mFALS mice), and knockout mice deficient in SOD1 (SOD1-KO). In addition, morphometric analysis was performed on the spinal cords of SOD1-KO and normal mice. RESULTS: In mFALS mice, the motor unit number in the distal hind limb declined before behavioral abnormalities appeared, and motor unit size increased. Compound motor action potential amplitude and distal motor latency remained normal until later in the disease. In SOD1-KO mice, motor unit numbers were reduced early but declined slowly with age. In contrast with the mFALS mice, SOD1-KO mice demonstrated only a modest increase in motor unit size. Morphometric analysis of the spinal cords from normal and SOD1-KO mice showed no significant differences in the number and size of motor neurons. CONCLUSIONS: The physiologic abnormalities in mFALS mice resemble those in human ALS. SOD1-deficient mice exhibit a qualitatively different pattern of motor unit remodeling that suggests that axonal sprouting and reinnervation of denervated muscle fibers are functionally impaired in the absence of SOD1.