Exposure to traumatic events at work, posttraumatic symptoms and professional quality of life among midwives.

OBJECTIVE: in their line of duty, midwives are often exposed to traumatic births that may lead to symptoms of compassion fatigue (CF), which includes burnout (BO) and secondary traumatic stress (STS).Conversely, midwives derive pleasure and great satisfaction in seeing the positive effect they have on their clients. This experience is known as compassion satisfaction (CS). Together, CS and CF comprise the professional quality of life (ProQOL). The aim of this paper was to study midwives' professional quality of life and traumatic experiences. The highly stressful environment of midwives may also include primary exposure to traumatic experiences and therefore PTSD levels were also assessed. METHOD: the participants (N=93) were professional midwives from four medical centers in Israel. The participants answered selfreport questionnaires that assessed their ProQOL and PTSD symptoms. FINDINGS: results indicated relatively high levels of CS which may mitigate, at least to some degree, the negative aspects of CF. PTSD levels significantly and positively correlated with STS and BO. Sixteen per cent presented with PTSD symptoms of clinical significance. Also, seniority was significantly and positively correlated with BO and PTSD symptoms. CONCLUSIONS: high ProQOL was found amongst the participants, with more than 74% scoring on the high range of CS. Nevertheless, we recommend further research and implementing strategies to maintain or further enhance CS and decrease CF levels. Finally, a more comprehensive understanding of the development of PTSD amongst midwives is vital in order to minimize its occurrence in the future.

Glutamate receptor antibodies directed against AMPA receptors subunit 3 peptide B (GluR3B) can be produced in DBA/2J mice, lower seizure threshold and induce abnormal behavior.

OBJECTIVE: Anti-GluR3B antibodies (GluR3B Ab's), directed against peptide B/aa372-395 of GluR3 subunit of glutamate/AMPA receptors, are found in ∼35% of epilepsy patients, activate glutamate/AMPA receptors, evoke ion currents, kill neurons and damage the brain. We recently found that GluR3B Ab's also associate with neurological/psychiatric/behavioral abnormalities in epilepsy patients. Here we asked if GluR3B Ab's could be produced in DBA/2J mice, and also modulate seizure threshold and/or cause behavioral/motor impairments in these mice. METHODS: DBA/2J mice were immunized with the GluR3B peptide in Complete Freund's Adjuvant (CFA), or with controls: ovalbumin (OVA), CFA, or phosphate-buffer saline (PBS). GluR3B Ab's and OVA Ab's were tested. Seizures were induced in all mice by the chemoconvulsant pentylenetetrazole (PTZ) at three time points, each time with less PTZ to avoid non-specific death. Behavior was examined in Open-Field, RotaRod and Grip tests. RESULTS: GluR3B Ab's were produced only in GluR3B-immunized mice, while OVA Ab's were produced only in OVA-immunized mice, showing high Ab's specificity. In GluR3B Ab's negative mice, seizure severity scores and percentages of animals developing generalized seizures declined in response to decreasing PTZ doses. In contrast, both parameters remained unchanged/high in the GluR3B Ab's positive mice, showing that these mice were more susceptible to seizures. The seizure scores associated significantly with the GluR3B Ab's levels. GluR3B Ab's positive mice were also more anxious in Open-Field test, fell faster in RotaRod test, and fell more in Grip test, compared to all the control mice. CONCLUSIONS: GluR3B Ab's are produced in DBA/2J mice, facilitate seizures and induce behavioral/motor impairments. This animal model can therefore serve for studying autoimmune epilepsy and abnormal behavior mediated by pathogenic anti-GluR3B Ab's.

Glutamate receptor antibodies directed against AMPA receptors subunit 3 peptide B (GluR3B) associate with some cognitive/psychiatric/behavioral abnormalities in epilepsy patients.

Antibodies (Ab's) to glutamate receptors, directed specifically against AMPA receptors subunit 3 peptide B (i.e. GluR3 amino acids 372-395), named GluR3B Ab's, can by themselves activate GluR3-containing glutamate/AMPA receptors, evoke ion currents via the receptor's ion channel, kill neurons and damage the brain. Herein we first tested 14 consecutive epilepsy patients and 10 healthy controls, and found that 7 (50%) patients had GluR3B Ab's. Second, in 71 other consecutive epilepsy patients (20 generalized epilepsy, 51 partial epilepsy) and 49 controls, we found that 17 (24%) patients had GluR3B Ab's, of which 8 had generalized and 9 partial epilepsy. We then studied 41 epilepsy patients: 21 patients with GluR3B Ab's and 20 without such Ab's (pooled of both tests without biased selection), for possible association of GluR3B Ab's with disease severity and/or neurobehavioral/cognitive comorbidities. Of the 21 patients with GluR3B Ab's, 6 had symptomatic, 7 cryptogenic, and 8 idiopathic epilepsy. Of the 20 patients without GluR3B Ab's, 16 had idiopathic etiology, and 4 nonidiopathic epilepsy. We found that among the 21 patients with GluR3B Ab's, 19 patients (90%) had learning problems, 16 (76%) attention problems, and 15 (71%) psychiatric problems. In contrast, among the 20 patients without GluR3B Ab's, only 6 (30%) had learning problems (p<0.0001), 5 (25%) attention problems (p=0.0017), and 2 (10%) psychiatric problems (p<0.0001). These findings suggest either that neurobehavioral abnormalities occur more frequently in epilepsy patients already having GluR3B Ab's, and may be due to them, or that GluR3B Ab's are more frequent in patients already having neurobehavioral abnormalities.