PubMed Health⌕ Search

Biomedical subjects

Patrick Berquin

Publications and source records attributed to Patrick Berquin.

4 recordsLinked to original sources

Cardiorespiratory effects induced by vagus nerve stimulation in epileptic children.

Vagus nerve stimulation (VNS) is used in pharmaco-resistant epilepsy to decrease the number of seizures. Although it is well known that VNS affects respiration, there are only a few reports concerning an effect of VNS on heart rate or heart rate variability (HRV). We investigated the relationship between respiratory frequency and the high frequency (HF) domain of the discrete Fourier transform (DFT) of the RR interval function during night sleep recordings of ten subjects treated with VNS. Our results show that VNS shifts the frequency of maximal power spectrum density (PSD) in the HF-band, decreases the related PSD and induces a partial cardiorespiratory decoupling.

Adolescent↗

Vagus nerve stimulation induces concomitant respiratory alterations and a decrease in SaO2 in children.

PURPOSE: To analyze respiratory alterations and effects on SaO(2) caused by vagus nerve stimulation (VNS) in children with epilepsy. METHODS: Polysomnographic recordings, including electroencephalography, thoracoabdominal distention, nasal airflow, SaO(2), and VNS artifact were evaluated in 10 children with pharmacoresistant epilepsy treated with VNS. RESULTS: Each VNS caused a significant increase in respiratory frequency (p < 0.05) throughout the stimulation period and a decrease in thoracoabdominal-distention amplitude (p < 0.05), especially at the beginning of the stimulation. These respiratory alterations induced a decrease in SaO(2) from 1 to 5%. The effects of VNS on respiration differed significantly between rapid-eye-movement (REM) and non-REM (NREM) sleep states. CONCLUSIONS: VNS caused a pronounced change in respiration in children with epilepsy, and this induced a decrease in SaO(2). It is possible that VNS has a neuroprotective effect, and this possibility calls for further investigation.

Adolescent↗

Chronic infantile neurological cutaneous and articular syndrome is caused by mutations in CIAS1, a gene highly expressed in polymorphonuclear cells and chondrocytes.

Chronic infantile neurological cutaneous and articular (CINCA) syndrome is a severe chronic inflammatory disease of early onset, characterized by cutaneous symptoms, central-nervous-system involvement, and arthropathy. In the present study, we report, in seven unrelated patients with CINCA syndrome, distinct missense mutations within the nucleotide-binding site of CIAS1, a gene encoding cryopyrin and previously shown to cause Muckle-Wells syndrome and familial cold urticaria. Because of the severe cartilage overgrowth observed in some patients with CINCA syndrome and the implications of polymorphonuclear cell infiltration in the cutaneous and neurological manifestations of this syndrome, the tissue-specific expression of CIAS1 was evaluated. A high level of expression of CIAS1 was found to be restricted to polymorphonuclear cells and chondrocytes. These findings demonstrate that CIAS1 missense mutations can result in distinct phenotypes with only a few overlapping symptoms and suggest that this gene may function as a potential inducer of apoptosis.

Amino Acid Sequence↗