Berghelms6446

erol.Lyme disease is a multi-faceted illness caused by infection due to Borrelia burgdorferi. Acute kidney damage secondary to Lyme disease is well described but less so as a chronic event. The role of Anaplasma spp. and secondary kidney dysfunction is not known. A retrospective cohort study was performed to determine if dogs within a defined Lyme disease and anaplasmosis region with B. burgdorferi or Anaplasma spp. antibodies had an increased risk of chronic kidney disease (CKD). Patient exposure was defined as having a B. burgdorferi or Anaplasma spp. antibody positive result recorded at any point in the available patient history. CKD was defined as concurrent increased symmetric dimethylarginine and creatinine (Cr) for a minimum of 25 days with inappropriate urine specific gravity (USG). Patients were matched using propensity scoring to control for age, region, and breed. Contingency tables were used to compare dogs seropositive and not seropositive to B. burgdorferi and Anaplasma spp. and CKD outcome. For each comparison that was performed, statistical significance was defined by a P-value of less then .025. The risk ratio of CKD for patients exposed to B. burgdorferi and Anaplasma spp. were found to be 1.43 (95% confidence interval [CI, 1.27, 1.61], P less then .0001) and 1.04, (95% CI [0.87, 1.24], P = .6485), respectively. Results suggest in this cohort no increased risk for developing CKD when exposed to Anaplasma spp. but a significant increase in risk for developing CKD with exposure to B. burgdorferi.

Monitoring of the ultra-low frequency potentials, particularly cortical spreading depression (CSD), is excluded in epilepsy monitoring due to technical barriers imposed by the scalp ultra-low frequency electroencephalogram (EEG). As a result, clinical studies of CSD have been limited to invasive EEG. see more Therefore, the occurrence of CSD and its interaction with epileptiform field potentials (EFP) require investigation in epilepsy monitoring.

Using a novel AC/DC-EEG approach, the occurrence of DC potentials in patients with intractable epilepsy presenting different symptoms of aura was investigated during long-term video-EEG monitoring.

Various forms of slow potentials, including simultaneous negative direct current (DC) potentials and prolonged EFP, propagated negative DC potentials, and non-propagated single negative DC potentials were recorded from the scalp of the epileptic patients. The propagated and single negative DC potentials preceded the prolonged EFP with a time lag and seizure appeared at the final shoulder of some instances of the propagated negative DC potentials. The slow potential deflections had a high amplitude and prolonged duration and propagated slowly through the brain. The high-frequency EEG was suppressed in the vicinity of the negative DC potential propagations.

The study is the first to report the recording of the propagated and single negative DC potentials with EFP at the scalp of patients with intractable epilepsy. The negative DC potentials preceded the prolonged EFP and may trigger seizures. The propagated and single negative DC potentials may be considered as CSD.

Recordings of CSD may serve as diagnostic and prognostic monitoring tools in epilepsy.

Recordings of CSD may serve as diagnostic and prognostic monitoring tools in epilepsy.

During motor execution (ME), mu power is diminished over the contralateral hemisphere and increased over the ipsilateral hemisphere, which has been associated with cortical activation of the contralateral motor areas and inhibition of the ipsilateral motor areas respectively. The influence of action observation (AO) and motor imagery (MI) on mu power is less clear, especially in children, and remains to be studied in children with unilateral cerebral palsy (uCP).

We determined mu power during ME, AO, and MI of 45 typically developing (TD) children and 15 children with uCP over both hemispheres, for each hand.

In TD children, over the left hemisphere mu power was lowered during ME when the right hand was used. In line, over the right hemisphere mu power was lowered when the left hand was addressed. In addition, during AO and MI increased mu power was observed when the right hand was addressed. In children with uCP, over the spared hemisphere mu power was diminished during ME when the less-affected hand was used. However, over the lesioned hemisphere, no mu changes were observed.

The results of TD children fit the activation/inhibition model of mu power.

The results of children with uCP suggest that the lesioned hemisphere is unresponsive to the motor tasks.

The results of children with uCP suggest that the lesioned hemisphere is unresponsive to the motor tasks.

The patient acceptable symptom state (PASS) is a treatment-response criterion developed to determine the clinical relevance of a treatment effect. Its estimates for some patient-reported outcomes (PROs) in non-specific chronic low back pain (cLBP) are lacking and the stability of PRO estimates between independent cLBP populations is unknown. We hypothesized that these PRO estimates will be stable.

To estimate and compare the PASS for PROs between 2 independent cLBP populations.

We conducted a secondary analysis of a randomized controlled trial (PREDID) and a cohort of outpatients with non-specific cLBP. Using an anchoring question, participants who self-rated their health as "excellent", "very good" or "good" at 1 month were considered to have an acceptable symptom state. PASS estimates for 5 PROs were calculated by using the 75th percentile method. Estimates were compared between the 2 populations with bootstrap resampling.

A total of 256 participants with non-specific cLBP were included 135 patientsues in clinical trials and practice. ClinicalTrials.gov no. (PREDID trial) NCT00804531.

Our study provides PASS estimates for 5 PROs commonly used in cLBP. Our estimates were stable between 2 independent populations of people with cLBP. The stability of our PASS estimates suggests that they are relevant for interpreting PRO values in clinical trials and practice. ClinicalTrials.gov no. (PREDID trial) NCT00804531.