Neuroanatomy of coprolalia in Tourette syndrome using functional magnetic resonance imaging

OBJECTIVE: To determine the neural substrates of phonic tics in Tourette syndrome (TS) using functional magnetic resonance imaging (fMRI) and compare with a proposed tic-generating network (TGN). PATIENTS: One with TS and one normal control. METHODS: fMRI scans were obtained on the TS patient during which numerous unsuppressed phonic tics occurred and, along with the scanner noise, were recorded on audiotape. The control underwent the same functional MRI sequence but mimicked the tics within predetermined, on-off time blocks. Fuzzy clustering (FC) methods were used to generate the activation maps. RESULTS: The TS patient and control showed fMRI activation in the left middle frontal gyrus and right precentral gyrus. The TS patient also had activity in the caudate nucleus, cingulate gyrus, cuneus, left angular gyrus, left inferior parietal gyrus, and occipital gyri. CONCLUSIONS: fMRI, using an FC analysis, is a viable technique for studying TS patients with phonic tics. These results give further support to the hypothesis of a tic-generating circuit model. Further studies are required to confirm our data.     

Cytological criteria to predict basal phenotype of breast carcinomas

Breast carcinoma is a heterogeneous disease. It can be classified into phenotypes based on the expression of certain proteins, with distinct differences in prognosis. The basal phenotype is associated with worse prognosis and it still remains without specific treatment. However, there is currently no international consensus on the cytological criteria that could predict this phenotype. The purpose of the study was to evaluate the cytological criteria in fine‐needle aspiration biopsy and to identify their association with the basal phenotype of breast carcinoma. Fine‐needle aspiration biopsy specimens and tissue sections (mastectomy specimen) from 74 cases of high‐grade invasive ductal breast carcinomas were consecutively retrieved from the files of three institutions. Breast carcinomas were studied using the tissue microarray technique, being classified into phenotypes: luminal A, luminal B, HER2 overexpression, and basal. The cytological criteria for all cases were reviewed blindly by two pathologists according to five cytological criteria: cellularity, cell pattern, presence of necrosis, nucleoli, and nuclear atypia. Exact Fisher test was used to test the association between cytological criteria and the phenotypes of breast carcinoma. Necrosis was present in 64.7% of basal breast carcinomas, and 31.1% of nonbasal breast carcinomas, and that result was statistically significant, showing an odds ratio (OR) of 3.80. The basal phenotype, compared with the luminal A, showed more necrosis (OR = 6.97), present/prominent nucleoli (OR = 8.18), and cellularity more frequently (OR = 18.03). Necrosis, as well as present/prominent nucleoli and abundant cellularity are criteria more frequently associated to the basal phenotype of breast carcinoma. Diagn. Cytopathol. 2009. © 2009 Wiley‐Liss, Inc.     

Effect of angiotensin and norepinephrine on capillary pressure and filtration coefficient in isolated dog hindlimb

Using the isogravimetric technique quantitative measurements were made of changes in precapillary (R_A) and postcapillary (R_V) resistances, mean capillary pressure (P_C), and filtration coefficients (K_f) in isolated dog hindlimbs perfused under conditions of constant pressure or constant flow during intraarterial infusion of angiotensin and norepinephrine. For constant pressure perfusion both angiotensin and norepinephrine initially produced an increase in R_A and R_V while P_C fell below control. Subsequently, R_A decreased toward control, R_v remained constant, and P_C increased and stabilized at control value. For constant flow perfusion R_A, R_V, and P_C increased and remained elevated during both angiotensin and norepinephrine infusion. Twenty minutes after onset of drug infusion, K_f was above control for angiotensin but was not significantly different from control for norepinephrine. Since capillary permeability to protein was not altered by either agent, the increase in K_f during angiotensin infusion presumably results from an increase in capillary surface area available to fluid movement, and suggests that during prolonged infusion of these agents (>20 min) the vasoconstriction thus produced may not compromise capillary blood flow to skeletal muscle.     

Risk factors and clinical profile of thrombotic thrombocytopenic purpura in systemic lupus erythematosus patients. Is this a distinctive clinical entity in the thrombotic microangiopathy spectrum?: A case control study

Introduction

The association of thrombotic thrombocytopenic purpura (TTP) with systemic lupus erythematosus (SLE) is rare. It is associated with high morbidity and mortality. Information about risk factors and clinical outcomes is scant.

Material and Methods

A retrospective case-control study was performed in a referral center in Mexico City between 1994 and 2013. Patients were diagnosed with TTP if they fulfilled the following criteria: microangiopathic haemolytic anaemia, thrombocytopenia, high LDH levels, normal fibrinogen and negative Coombs’ test. Patients with SLE were diagnosed with ≥ 4 ACR criteria. We included three study groups: group A included patients with SLE-associated TTP (TTP/SLE; cases n = 22, TTP events n = 24); patients with non-autoimmune TTP (NA-TTP; cases n = 19, TTP events n = 22) were included in group B and patients with SLE without TTP (n = 48) in group C.

Results

After multivariate analysis, lymphopenia < 1000/mm3 [OR 19.84, p = 0.037], high SLEDAI score three months prior to hospitalisation [OR 1.54, p = 0.028], Hg < 7 g/dL [OR 6.81, p = 0.026], low levels of indirect bilirubin [OR 0.51, p = 0.007], and less severe thrombocytopenia [OR 0.98, p = 0.009] were associated with TTP in SLE patients. Patients with TTP/SLE received increased cumulative steroid dose vs. NA-TTP (p = 0.006) and a higher number of immunosuppressive drugs (p = 0.015). Patients with TTP/SLE had higher survival than NA-TTP (p = 0.033); however, patients hospitalised for TTP/SLE had a higher risk of death than lupus patients hospitalised for other causes

Conclusions

Lymphopenia is an independent risk factor for TTP/SLE. It is likely that patients with TTP/SLE present with less evident clinical features, so the level of suspicion must be higher to avoid delay in treatment.     

Small and large fiber sensory polyneuropathy in type 2 diabetes: Influence of diagnostic criteria on neuropathy subtypes

Diabetic polyneuropathy (DPN) can be classified based on fiber diameter into three subtypes: small fiber neuropathy (SFN), large fiber neuropathy (LFN), and mixed fiber neuropathy (MFN). We examined the effect of different diagnostic models on the frequency of polyneuropathy subtypes in type 2 diabetes patients with DPN. This study was based on patients from the Danish Center for Strategic Research in Type 2 Diabetes cohort. We defined DPN as probable or definite DPN according to the Toronto Consensus Criteria. DPN was then subtyped according to four distinct diagnostic models. A total of 277 diabetes patients (214 with DPN and 63 with no DPN) were included in the study. We found a considerable variation in polyneuropathy subtypes by applying different diagnostic models independent of the degree of certainty of DPN diagnosis. For probable and definite DPN, the frequency of subtypes across diagnostic models varied from: 1.4% to 13.1% for SFN, 9.3% to 21.5% for LFN, 51.4% to 83.2% for MFN, and 0.5% to 14.5% for non‐classifiable neuropathy (NCN). For the definite DPN group, the frequency of subtypes varied from: 1.6% to 13.5% for SFN, 5.6% to 20.6% for LFN, 61.9% to 89.7% for MFN, and 0.0% to 6.3% for NCN. The frequency of polyneuropathy subtypes depends on the type and number of criteria applied in a diagnostic model. Future consensus criteria should clearly define sensory functions to be tested, methods of testing, and how findings should be interpreted for both clinical practice and research purpose.     

Developing a Sound Body: Open Trial Results of a Group Healthy Lifestyle Intervention for Young Adults with Psychosis

Community Mental Health Journal - The mortality disparity for persons with schizophrenia spectrum disorders (SSDs) due to cardiovascular disease is a devastating problem. Many risk factors are...     

Indirect treatment comparison of new oral anticoagulants for the treatment of acute venous thromboembolism

Background

Numerous new oral anticoagulants (NOACs) have been compared to a parenteral anticoagulant/oral vitamin K antagonist (VKA) for the treatment of acute venous thromboembolism (VTE). We aimed to conduct a systematic review and adjusted indirect comparison meta-analysis to compare the efficacy and safety of NOACs for this indication.

Methods

We conducted a systematic literature search through November 2013 for randomized trials that evaluated treatment of acute VTE with a NOAC including rivaroxaban, apixaban, dabigatran and edoxaban. Trials had to report at least one of the following outcomes of interest: mortality, recurrent VTE, recurrent pulmonary embolism (PE), recurrent deep vein thrombosis (DVT), or major bleeding. Included trials were evaluated for quality using the Cochrane Risk of Bias tool. We performed an adjusted indirect comparison meta-analysis to evaluate the comparative efficacy and safety of NOACs, reporting relative risks (RRs) and 95% confidence intervals for each outcome.

Results

Six trials (n = 27,069) met inclusion criteria, one each evaluating apixaban and edoxaban and two trials each evaluating rivaroxaban and dabigatran. Risk of bias was low for all trials. NOACS did not differ significantly in the risk of mortality, recurrent VTE, recurrent PE or recurrent DVT. Dabigatran increased major bleeding risk compared to apixaban [RR 2.69 (1.19 to 6.07)] as did edoxaban compared to apixaban [RR 2.74 (1.40 to 5.39)].

Conclusion

Although NOACs do not appear to differ in the efficacy of treating acute VTE, data suggests apixaban to be the safer than some of its competitors.     

Tumor-like enlargement of the optic chiasm in an infant with Alexander disease

We report a patient with infantile Alexander disease (AXD) due to the recurrent p.Arg79Cys GFAP mutation. In addition to typical AXD abnormalities, magnetic resonance imaging demonstrated a tumor-like lesion of the optic chiasm suggestive of a glioma. A transient papilloedema appeared during the follow-up and the lesion partially regressed despite a worsening of white matter involvement. Rare radiological and pathological tumor-like lesions have already been reported in AXD patients. This patient confirms that enlargement of the optic chiasm is a rare feature of AXD, possibly linked to abnormal astrocytic proliferation.     

Apamin induces plastic changes in hippocampal neurons in senile Sprague-Dawley rats

Apamin is a neurotoxin extracted from honey bee venom and is a selective blocker of small‐conductance Ca²⁺‐activated K⁺ channels (SK). Several behavioral and electrophysiological studies indicate that SK‐blockade by apamin may enhance neuron excitability, synaptic plasticity, and long‐term potentiation in the CA1 hippocampal region, and, for that reason, apamin has been proposed as a therapeutic agent in Alzheimer's disease treatment. However, the dendritic morphological mechanisms implied in such enhancement are unknown. In the present work, Golgi–Cox stain protocol and Sholl analysis were used to study the effect of apamin on the dendritic morphology of pyramidal neurons from hippocampus and the prefrontal cortex as well as on the medium spiny neurons from the nucleus accumbens and granule cells from the dentate gyrus (DG) of the hippocampus. We found that only granule cells from the DG and pyramidal neurons from dorsal and ventral hippocampus were altered in senile rats injected with apamin. Our research suggests that apamin may increase the dendritic morphology in the hippocampus, which could be related to the neuronal excitability and synaptic plasticity enhancement induced by apamin. Synapse 2011. © 2011 Wiley‐Liss, Inc.