Protein tyrosine phosphatase receptor type Q in cerebrospinal fluid reflects ependymal cell dysfunction and is a potential biomarker for adult chronic hydrocephalus.

BACKGROUND AND PURPOSE: Protein tyrosine phosphatase receptor type Q (PTPRQ) was extracted from the cerebrospinal fluid (CSF) of patients with probable idiopathic normal-pressure hydrocephalus (iNPH) by proteome analysis. We aimed to assess the feasibility of using CSF PTPRQ concentrations for the additional diagnostic criterion of iNPH in Japanese and Finnish populations. METHODS: We compared PTPRQ concentrations among patients with probable iNPH and neurologically healthy individuals (normal control [NC] group), patients with normal-pressure hydrocephalus (NPH) of acquired and congenital/developmental aetiologies, patients with Alzheimer's disease and patients with Parkinson's disease in a Japanese analysis cohort. A corresponding iNPH group and NC group in a Finnish cohort was used for validation. Patients in the Finnish cohort who underwent biopsy were classified into two groups based on amyloid and/or tau deposition. We measured PTPRQ expression levels in autopsied brain specimens of iNPH patients and the NC group. RESULTS: Cerebrospinal fluid PTPRQ concentrations in the patients with NPH of idiopathic, acquired and congenital/developmental aetiologies were significantly higher than those in the NC group and those with Parkinson's disease, but iNPH showed no significant differences when compared with those in the Alzheimer's disease group. For the patients with iNPH, the area under the receiver-operating characteristic curve was 0.860 in the Japanese iNPH and 0.849 in the Finnish iNPH cohorts. Immunostaining and in situ hybridization revealed PTPRQ expression in the ependymal cells and choroid plexus. It is highly possible that the elevated PTPRQ levels in the CSF are related to ependymal dysfunction from ventricular expansion. CONCLUSIONS: Cerebrospinal fluid PTPRQ levels indicated the validity of this assay for auxiliary diagnosis of adult chronic hydrocephalus.

The effect of two different doses of remifentanil on postoperative pain and opioid consumption after cardiac surgery--a randomized controlled trial.

BACKGROUND: Remifentanil, an ultra-short-acting opioid, provides intensive analgesia without prolonged respiratory depression and is widely used in cardiac surgery. Diminished dosing may also offer stable hemodynamics, even during sternotomy and sternal retraction. However, increased postoperative pain and induced opioid tolerance after remifentanil dosing during abdominal surgery was reported. We tested whether remifentanil 0.3 µg/kg/min infusion increased postoperative opioid consumption and pain compared to 0.1 µg/kg/min dosing. METHODS: Ninety coronary artery bypass grafting or heart valve surgery patients were randomized to remifentanil 0.1 µg/kg/min or 0.3 µg/kg/min infusions during surgery. All patients received oxycodone bolus 0.15 µg/kg postoperatively, and patient-controlled analgesia (PCA) with oxycodone thereafter. Postoperative pain was estimated thrice daily by visual analogue scale, and 48-h opioid consumption was recorded from the PCA-device. RESULTS: Total remifentanil dosing was 64 µg/kg in the higher and 22 µg/kg in the lower dosing group during the 3-h cardiac operations. Mean postoperative opioid consumption was 107 (SD 36) mg in the lower and 104 (SD 33) mg in the higher dose remifentanil groups. Postoperative pain did not differ between groups, at rest or during deep breathing, at any time (P = 0.110 and 0.941, respectively). CONCLUSIONS: Remifentanil 0.3 µg/kg/min infusion did not increase postoperative pain or opioid consumption after cardiac surgery compared to the 0.1 µg/kg/min infusion. Remifentanil infusion 0.1-0.3 µg/kg/min during cardiac surgery was safe, with no exaggerated postoperative pain or opioid consumption.

Auditory-evoked potentials in bispectral index-guided anaesthesia for cardiac surgery.

BACKGROUND AND OBJECTIVE: Midlatency auditory-evoked potentials, as measures of the anaesthetic state, were evaluated at similar levels of bispectral index in cardiac surgical patients maintained with either propofol or isoflurane anaesthesia. METHODS: Twenty-four patients were randomly allocated to anaesthesia with propofol (n = 12) or isoflurane (n = 12). Bispectral index was maintained below 60 during surgery. Auditory-evoked potentials were collected before induction of anaesthesia, 10 min after intubation, 30 min after sternotomy, during cardiopulmonary bypass at the time of cross-clamping of the aorta and during stable mild hypothermia, after de-clamping of the aorta, and after the operation. RESULTS: At the pre-determined time points, bispectral index values showed comparable depth of hypnosis in both groups. The latency of the Nb component of midlatency auditory-evoked potentials was significantly increased in the isoflurane group after intubation (P < 0.001) and that of both the Nb and the Pa components after sternotomy (P < 0.001) compared with the propofol group. No differences between the groups were detected with respect to haemodynamic variables. No patient reported recall of intraoperative events. CONCLUSION: After intubation and surgical stimulation, when bispectral index was at a constant level, there was a difference in the Nb and Pa components of the midlatency auditory-evoked potentials between the two anaesthetic regimens, indicating a distinction in the state of anaesthesia. Our results suggest that the parallel use of these two electrophysiological methods can show differences in the components of anaesthesia between various anaesthesia methods in cardiac surgical patients.

Recovery of N100 component of auditory event-related potentials and EEG after cardiac arrest during propofol sedation.

We report on the EEG monitoring of a patient who suffered an episode of postoperative ventricular fibrillation (VF) following coronary artery bypass grafting (CABG). VF initially caused a considerable suppression and slowing of the EEG. The recovery of cerebral function was evaluated by recording both EEG and auditory event related potentials (ERPs). Six hours after the episode of VF, when the patient was asleep but arousable to voice command, the N100 component of the auditory ERPs had recovered to the level measured before the operation, whereas the EEG was still very slow for that level of sedation. This may have been due to VF having less effect on the N100 component than on the background EEG. Our findings suggest that measuring evoked potentials may improve the evaluation of brain function after cardiac arrest.