Fetal intracranial hemorrhage related to maternal autoimmune thrombocytopenic purpura

Background

Maternal autoimmune thrombocytopenic purpura (AITP) can cause fetal intracranial hemorrhage.

Case report

A 19-year-old primigravida was referred to our institution for prenatally detected ventriculomegaly at 30th week of gestation. Her personal and family histories were unremarkable. Her platelet count was 54?×?109/L. Fetal neurosonography showed intraparenchymal hemorrhage. AITP was diagnosed in the mother and platelet count decreased at 34?×?109/L. Patient was treated with methylprednisolone and intravenous immunoglobulin. She delivered a 2,340-g infant at 37 weeks with elective cesarean section. The platelet count of the newborn was 181?×?109/L and coagulation tests were normal. No antiplatelet specific antibodies were detected in cord blood. Postnatal MRI evaluation confirmed grade IV intracranial hemorrhage. The newborn baby has suffered from mild spasticity and seizures.

Conclusions

Clinicians must be vigilant about the catastrophic fetal complications of maternal AITP; a close follow-up with a multidisciplinary cooperation between obstetricians, hematologists, and neonatologists must be warranted.     

Neurological complication of non Hodgkin lymphoma in childhood: experience from a single center in Turkey

Purpose

Lymphomas are the third most common childhood malignant disease after leukemia and central nervous system (CNS) tumors. Early diagnosis of these complications will reduce mortality and morbidity. In this study we aimed to review the neurological complications of childhood non Hodgkin Lymphoma (NHL).

Patients and methods

Forty four children with NHL between 2006 and 2012 were investigated retrospectively and 14 cases with neurological complications were identified.

Results

The most common symptom was alteration of the consciousness (10 patients, 71.4 %) followed by convulsion (5 patients, 35.7 %), and hallucination (4 patients, 28.5 %); headache, eye pain, neurogenic bladder, speech disability and facial paralysis, and hemiplegia, were less common and each of them was seen in 1 (7.1 %) of the patients. The neurological complications were mostly seen in children with precursor T lymphoblastic lymphoma followed by anaplastic large cell lymphoma. The complications were secondary to medications (Eight patients) infection (two patients); CNS relapse (two patients); or CNS involvement of the primary disease (two patients). Chemotherapy-related neurologic complications were secondary to intrathecal methotrexate, l-asparaginase, vincristine, and ifosfamide

Conclusion

Advanced disease and PTLL subtype can be suggested as predictors of neurological complication. The survival rates of neurological complications are fairly good unless it is secondary to involvement of the primary disease. In patients with drug-induced neurological complications, the treatment can be safely re-administered after controlling the neurological complications. Therefore, clinicians managing children with NHL must be informative about neurological complications.     

Cortical inputs innervate calbindin‐immunoreactive interneurons of the rat basolateral amygdaloid complex

The present study was undertaken to shed light on the synaptic organization of the rat basolateral amygdala (BLA). The BLA contains multiple types of GABAergic interneurons that are differentially connected with extrinsic afferents and other BLA cells. Previously, it was reported that parvalbumin immunoreactive (PV⁺) interneurons receive strong excitatory inputs from principal BLA cells but very few cortical inputs, implying a prevalent role in feedback inhibition. However, because prior physiological studies indicate that cortical afferents do trigger feedforward inhibition in principal cells, the present study aimed to determine whether a numerically important subtype of interneurons, expressing calbindin (CB⁺), receives cortical inputs. Rats received injections of the anterograde tracer Phaseolus vulgaris‐leucoagglutinin (PHAL) in the perirhinal cortex or adjacent temporal neocortex. Light and electron microscopic observations of the relations between cortical inputs and BLA neurons were performed in the lateral (LA) and basolateral (BL) nuclei. Irrespective of the injection site (perirhinal or temporal neocortex) and target nucleus (LA or BL), ～90% of cortical axon terminals formed asymmetric synapses with dendritic spines of principal BLA neurons, while 10% contacted the dendritic shafts of presumed interneurons, half of which were CB⁺. Given the previously reported pattern of CB coexpression among GABAergic interneurons of the BLA, these results suggest that a subset of PV‐immunonegative cells that express CB, most likely the somatostatin‐positive interneurons, are important mediators of cortically evoked feedforward inhibition in the BLA. J. Comp. Neurol. 522:1915–1928, 2014. © 2013 Wiley Periodicals, Inc.     

Pituitary volume in patients with panic disorder

Panic patients have many functional deficiencies in the hypothalamic-pituitary-adrenal (HPA) axis. Previous studies have shown changed pituitary gland volume in some psychiatric disorders that have functional deficiencies in the HPA axis. However, to date no study has evaluated the pituitary gland volume in patients with panic disorder (PD). We investigated the pituitary gland volume in patients with PD (n = 27) and age- and sex-matched healthy controls (n = 27), using 1.5-T magnetic resonance imaging in this study. Analysis showed that patients with PD had significantly smaller pituitary volume compared to healthy subjects. Patients with agoraphobia especially had a significantly smaller pituitary volume than patients without agoraphobia. There was a significant relationship between the pituitary volume and both the severity of symptoms and the illness duration in the patient group. The results show that patients with PD have reduced pituitary volume, which may reflect the functional abnormalities seen in this disorder. These findings may help us better understand the pathology of PD.     

Acute and chronic effects of electroconvulsive treatment on oxidative parameters in schizophrenia patients

Electroconvulsive therapy (ECT) is an effective treatment alternative for schizophrenia. Previous studies have already indicated the possible effects of oxidative stress in this disorder. However, there have been no previous studies evaluating the effects of ECT on the oxidative stress in these patients. We therefore aimed to investigate the acute and chronic effects of ECT on serum levels of oxidant and antioxidant molecules in schizophrenia patients (n = 28). The serum MDA and CAT levels of the patients with schizophrenia were higher than that of the controls before ECT (n = 20) but there was no significant difference in the serum NO and GSH levels of the patient groups compared to the controls. We found that the NO levels of the patients were higher than the controls in the group experiencing their first episode but not in the chronic group. There was a significant clinical improvement in the patients in terms of BPRS, SANS and SAPS reduction after the 9th ECT, but not the 1st ECT. Serum MDA levels were significantly reduced compared to the baseline after the 9th ECT session although there was no significant difference after the 1st session. Separate evaluation of the patient groups revealed that the significant MDA decrease following ECT was in the patients experiencing their first episode and not in the chronic group. No significant difference was noted in the serum levels of other oxidant and antioxidant molecules after either the 1st or 9th ECT session. These results suggest that ECT does not produce any negative effect on oxidative stress in patients with schizophrenia.