Continuous EEG-SEP monitoring of severely brain injured patients in NICU: methods and feasibility.

AIMS: To evaluate the feasibility of a continuous neurophysiologic monitoring (electroencephalography (EEG)-somatosensory evoked potentials (SEPs)) in the neuro-intensive care unit (NICU), taking into account both the technical and medical aspects that are specific of this environment. METHODS: We used an extension of the recording software that is routinely used in our unit of clinical neurophysiology. It performs cycles of alternate EEG and SEP recordings. Raw traces and trends are simultaneously displayed. Patient head and stimulator box are placed behind the bed and linked to the ICU monitoring terminal through optic fibers. The NICU staff has been trained to note directly clinical events, main artefacts and therapeutic changes. The hospital local area network (LAN) enables remote monitoring survey. RESULTS: Continuous EEG (CEEG)-SEP monitoring was performed in 44 patients. Problems of needle detachment were seldomly encountered, thanks to the use of a sterile plastic dressing, which covers needles. We never had infection or skin lesions due to needles or the electrical stimulator. The frequent administration of sedative at high doses prevented us from having a clinically valuable EEG in several cases but SEPs were always monitorable, independently of the level of EEG suppression. The diagnosis of seizures and non-epileptic status was based on raw EEG, while quantitative EEG (QEEG) was used to quantify ictal activity as a guide to treatment. CONCLUSIONS: EEG and EP waveforms collected in NICU were of comparable quality to routine clinical measurements and contained the same clinical information. A continuous SEP monitoring in a comatose and sedated patient in NICU is not technically more difficult and potentially less useful than in operating room. This monitoring appears to be feasible provided the observance of some requirement regarding setting, electrodes, montages, personnel integration, consulting and software.

Evaluation of short-term low-dose triple therapy for the eradication of Helicobacter pylori by factorial design in a randomized, double-blind, controlled study.

BACKGROUND: Studies demonstrating the efficacy of short-term low-dose triple therapies including omeprazole (O), clarithromycin (C) and a nitroimidazole (tinidazole, T) for Helicobacter pylori eradication have largely been open and uncontrolled, and have not assessed antibiotic sensitivity. Simpler regimens using the component drugs have not been evaluated. AIM: To evaluate the OCT regimen in a randomized, controlled trial, testing for pre- and post-treatment antibiotic resistance and comparing, in a factorial design, the OCT regimen with simpler combinations of its components. METHODS: One hundred and twenty-eight patients (68 males, 60 females, age 22-80 years, mean 53 years) with H. pylori gastritis were randomly assigned to one of the following four treatment groups: (C) clarithromycin 250 mg b.d.; (OC) omeprazole 20 mg o.d. + clarithromycin 250 mg b.d.; (CT) clarithromycin 250 mg b.d. + tinidazole 500 mg b.d.; (OCT) omeprazole 20 mg q.d.s. + clarithromycin 250 mg b.d. + tinidazole 500 mg b.d. The drugs were administered for 1 week. Medical interview, upper gastrointestinal endoscopy (with four antral and four corpus biopsies) and the 13C-urea breath test were carried out for all patients prior to and 4 weeks after treatment. Biopsy specimens were used for the urease test, histology, and culture and sensitivities. RESULTS: All but one patient completed treatment. Side-effects were rare and mild in all groups. The eradication rate was 93.8% in group OCT, 59.4% in group CT, 31.3% in group OC and 6.3% in group C. Pre-treatment metronidazole resistance was 12.8%, clarithromycin 1.1% and, to both antibiotics, 2.1%. In patients with pre-treatment metronidazole resistance, the eradication rate was 75% in group OCT and 33% in group CT. Post-treatment resistance to clarithromycin was induced in 28.5% of the failures in group C, but in none of group OC. Resistance to both antibiotics occurred in 22.2% of the failures in group CT and in none of group OCT. CONCLUSIONS: (i) The high efficacy of the OCT regimen is proved and each of the individual components of the regimen is essential to the result, possibly via a synergistic effect. (ii) Pre-treatment metronidazole resistance is scarcely relevant to the outcome. (iii) Acquired resistance is essentially nil if omeprazole is part of the regimen.

The Loiano-Monghidoro population-based study of Helicobacter pylori infection: prevalence by 13C-urea breath test and associated factors.

OBJECTIVES: As part of a cross-sectional study on cholelithiasis, 1533 out of 1840 residents in Loiano/Monghidoro, a rural area in Northern Italy (792 men, 741 women, age range 28-80 years), agreed to be further evaluated in relation to their Helicobacter pylori status. METHODS: Each participant performed a 13C-urea breath test (13C-UBT) and provided information on sociodemographic, lifestyle and clinical characteristics. RESULTS: The 13C-UBT was positive in 1041 subjects (67.9%; men: 69%; women: 67%) and was positively associated with increasing age (P < 0.001), alcohol consumption (P < 0.01), a higher number of siblings (P < 0.001) and a personal history of peptic ulcer (P < 0.01), but inversely with a nonmanual occupation (P < 0.001). Overall, H. pylori infection was unrelated to smoking, house pets, and a family history of gastroduodenal diseases. The prevalence of H. pylori infection was 72% in subjects reporting one or more dyspeptic symptoms and 65% among asymptomatic participants (P < 0.001); a multivariate analysis showed that only epigastric pain was significantly, although weakly, associated with 13C-UBT positivity. CONCLUSIONS: This large population-based study showed a prevalence of H. pylori infection higher than that reported by serologic surveys in urban areas. Current H. pylori infection was strongly associated with indicators of lower socioeconomic status, alcohol consumption and increasing age. A role of H. pylori infection in determining epigastric pain was suggested.

Low-dose lansoprazole and clarithromycin plus metronidazole vs. full-dose lansoprazole and clarithromycin plus amoxicillin for eradication of Helicobacter pylori infection.

AIM: To compare, in a randomized controlled trial, the efficacy and tolerability of two 1-week triple therapies for Helicobacter pylori eradication. METHODS: One hundred and thirty-four consecutive patients with non-ulcer dyspepsia and H. pylori infection were randomized to receive lansoprazole 30 mg once daily, clarithromycin 250 mg twice daily, and metronidazole 500 mg twice daily (LCM group), or lansoprazole 30 mg twice daily, clarithromycin 500 mg twice daily, and amoxicillin 1000 mg twice daily (LCA group). H. pylori status was assessed by rapid urease test, histology and 13C-urea breath test before and after therapy. RESULTS: At 3 months, H. pylori eradication (intention- to-treat/per protocol analysis) was 92.4%/93.8% in the LCM group and 83.1%/85.7% in the LCA group (P=N.S.). Side-effects were more frequently reported in the LCA group (37.9%) than in the LCM group (19.7%) (P < 0.05). CONCLUSIONS: In this open, randomized controlled trial, eradication of H. pylori by low-dose lansoprazole and clarithromycin plus metronidazole was higher with significantly less side-effects than by full-dose lansoprazole and clarithromycin plus amoxicillin. This finding may be related to the stronger synergism of clarithromycin plus metronidazole, even at lower doses, than of clarithromycin plus amoxicillin. Considering the lower cost as well, LCM should be preferred to LCA in the eradication of H. pylori.

Efficacy and safety of three 7-day Helicobacter pylori eradication regimens containing ranitidine bismuth citrate.

BACKGROUND: This multicentre, randomized study was designed to assess the clinical efficacy, safety and tolerability of three novel 7-day triple therapies containing ranitidine bismuth citrate (RBC) and two antibiotics. METHODS: We studied patients with non-ulcer dyspepsia and gastritis who were randomly assigned to one of three treatment regimens given for 7 days in a b.d. dosing schedule: RBC 400 mg plus clarithromycin 250 mg and tinidazole 500 mg (RBCCT): RBC 400 mg plus clarithromycin 500 mg and amoxycillin 1 g (RBCCA); RBC 400 mg plus tinidazole 500 mg and amoxycillin 1 g (RBCTA). H. pylori status was determined by CLO-test, histology and 13C-urea breath test. A repeat breath test was performed at least 28 days after completion of therapy to assess eradication. RESULTS: One hundred and fifty-seven patients were eligible for intention-to-treat analysis (ITT) and 140 patients completed the study and returned for assessment of eradication. Intention-to-treat cure rates were 78% with RBCCT, 71% with RBCCA and 61% with RBCTA. An all-patients-treated analysis (APT), performed on evaluable patients, demonstrated eradication rates of 85% with RBCCT, 81% with RBCCA and 70% with RBCTA. No statistically significant difference was found between treatment groups. Twenty-four patients experienced side-effects, but in only seven cases was treatment discontinued due to adverse events. CONCLUSIONS: A 7-day course of RBC, clarithromycin and either tinidazole or amoxycillin provides a good rate of H. pylori eradication. Three novel RBC-based triple therapies proved to be safe and well tolerated, with discontinuations due to side-effects occurring in less than 5% of cases.

Inhibin A, B and pro-alphaC in serum and peritoneal fluid in postmenopausal patients with ovarian tumors.

OBJECTIVE: To compare serum and peritoneal fluid concentrations of inhibin A, B, and pro-alphaC in women with ovarian tumors. METHODS: Serum and peritoneal fluid samples were taken from 41 postmenopausal women operated on for an ovarian tumor. Twenty-one patients with endometrial cancer formed a control group. Serum and peritoneal fluid inhibin A, B, and pro-alphaC concentrations, and serum FSH and tumor marker CA 125 (study group only) concentrations were analyzed. RESULTS: Inhibin A was found in low concentrations (median 4.1pg/ml, range <2-29pg/ml) in serum in most postmenopausal patients with epithelial ovarian carcinoma, whereas inhibin B was not measurable. Inhibin pro-alphaC circulated in high concentrations (median 125pg/ml, range 37->1000pg/ml). All inhibins were found in clearly greater concentrations in the peritoneal fluid than in serum. International Federation of Gynecology and Obstetrics (FIGO) stage III-IV and poor differentiation grade were associated with significantly lower concentrations of inhibin A and pro-alphaC in the peritoneal fluid compared with stages I-II or low grade. This correlation was not found in the serum concentrations of inhibin A or pro-alphaC. In the control group, no dimeric inhibins were found in serum, and pro-alphaC circulated in median concentrations of 47pg/ml (range 12-174pg/ml). CONCLUSIONS: Postmenopausal patients with epithelial ovarian tumors had low concentrations of inhibin A and relatively high concentrations of inhibin pro-alphaC in serum. The peritoneal fluid concentrations of all inhibins far exceeded those in the serum. Relatively low concentrations of inhibin A and pro-alphaC in the peritoneal fluid of patients with ovarian cancer seem to be associated with high stage and grade and, to a lesser degree, with positive peritoneal cytology.

Ovarian cancer and gonadotropins in vitro: new evidence in favor of independence.

BACKGROUND: The aim of this study was to investigate whether newly established epithelial ovarian carcinoma cell lines secrete inhibins, and whether their proliferative and secretory activity can be regulated by gonadotropins. MATERIALS AND METHODS: Three recently characterized human epithelial ovarian carcinoma cell lines were exposed to human choriongonadotropin hCG and follicle stimulating hormone FSH. Cell proliferation was determined by counting. Secretory activity of the cell lines was studied by analyzing inhibin A, inhibin B, inhibin pro-aC, estradiol, progesterone, testosterone, and CA 125 concentrations from the medium. The expression of gonadotropin receptors was studied by RT-PCR. RESULTS: None of the cell lines were found to secrete any of the inhibins, progesterone or testosterone. Only UT-OC-4 cells secreted low levels of estradiol. Gonadotropin receptors were not expressed by any of the cell lines, and accordingly neither FSH nor hCG stimulated the growth of these cells. However, hCG had some dose dependent growth inhibitory effect on UT-OC-3. Passage 42 cells of UT-OC-3 secreted significantly more CA 125 than passages 8 cells (P = 0.000). CONCLUSIONS: The present results suggest that the carcinomatous epithelial cells of the ovary do not secrete inhibins. The serum inhibin levels previously detected in patients with epithelial ovarian carcinoma may therefore reflect an ovarian stromal response to carcinoma. The findings are also in favor of an independence of ovarian cancer of gonadotropins.

What can be learnt from the new data about antibiotic resistance? Are there any practical clinical consequences of Helicobacter pylori antibiotic resistance?

Effective treatment regimens are now available for the eradication of Helicobacter pylori, but one of the factors limiting their efficacy is antibiotic resistance. Omeprazole-based triple therapy (omeprazole plus two antibiotics) can, at present, be considered the treatment of choice for H. pylori infection; some of the best results have been achieved by combining omeprazole with either amoxycillin and clarithromycin or metronidazole and clarithromycin. However, the potential effectiveness of nitroimidazole derivatives and clarithromycin must be weighed against the possibility that resistance can develop to these agents. Eradication in metronidazole-resistant strains is lower than in sensitive strains, but is still about 75% (versus 97%). However, clarithromycin resistance is thought to have more clinical significance, reducing the eradication rate of 95% in sensitive strains to 40% in resistant strains, although the overall importance of clarithromycin resistance for H. pylori eradication is still likely to be relatively low. Recent data on secondary resistance indicate that the rate is at least 50% for both metronidazole and clarithromycin in patients in whom eradication has failed. If, in the future, a large number of H. pylori-positive individuals undergo such treatment, treatment failures may become a major issue, and the problem of antibiotic resistance will have to be overcome.

Toremifene in postmenopausal breast cancer. Efficacy, safety and cost.

Toremifene is a chlorinated tamoxifen analogue that is indicated for the treatment of postmenopausal hormone-dependent breast cancer. It competes with estradiol for estrogen receptors and has growth-inhibitory effects on MCF-7 breast cancer cells. At concentrations < 10(-6) mol/L, this growth inhibition can be reversed by estradiol, but at higher concentrations toremifene is cytotoxic. In dimethylbenzanthracene (DMBA)-induced mammary cancer in rats, toremifene has been shown to decrease the number of new tumours and to inhibit the growth of existing tumours. Toremifene causes growth inhibition by suppressing mitosis and inducing apoptosis. The mechanism by which these events occur may involve the induction of transforming growth factor-beta 1 and inhibition of insulin-like growth factor-1 (mecasermin). Toremifene is primarily an antiestrogen, but it has some estrogen agonist properties in postmenopausal women. The latter are reflected by the fall in luteinising hormone and follicle-stimulating hormone levels and the rise in sex hormone-binding globulin levels that are associated with its use in most women. After estrogen priming, toremifene 68mg administered orally has been found to exert a similar antiestrogenic effect on the vaginal epithelium in postmenopausal women as tamoxifen 60mg. The half-life of toremifene in plasma is 5 days, and the drug is > 99% bound to plasma proteins. The main metabolites of toremifene are N-demethyl-toremifene and deaminohydroxy-toremifene. Altered liver, but not kidney, function affects the pharmacokinetics of toremifene. Toremifene 60mg daily is as effective as tamoxifen 20mg daily in the treatment of postmenopausal hormone-dependent breast cancer, producing a response in about 50% of patients. Soft tissue and visceral metastases respond better to toremifene than bone metastases. Most of the adverse effects of toremifene are related to its activity at estrogen receptors and include hot flashes, vaginal discharge and nausea. Although toremifene decreases antithrombin III levels slightly, the incidence of thromboembolic complications is low. Thus far, no carcinogenic effects have been noted in humans, and preclinical data are mostly reassuring. Toremifene has favourable effects on serum lipids, and thus has potential in preventing coronary heart disease. Although toremifene is somewhat more expensive to use than tamoxifen, toremifene is an effective and well tolerated alternative to tamoxifen in the treatment of postmenopausal women with hormone-dependent breast cancer. No formal pharmacoeconomic comparisons of toremifene and tamoxifen have yet been published. Toremifene is potentially safer than tamoxifen in relation to carcinogenic effects and effects on serum lipids.

Ovarian testosterone secretion during perimenopause.

OBJECTIVE: The aim of the study was to investigate ovarian testosterone secretion during the last few years of reproductive life and after menopause. MATERIALS AND METHODS: Ovarian and peripheral venous levels of total testosterone were analyzed in 52 women aged 42-69 years (mean 51) undergoing hysterectomy with adnexal removal for benign indications at the Department of Obstetrics and Gynecology at Tampere University Hospital, Finland. The study population was divided into pre- (n = 19), peri- (n = 18) and postmenopausal (n = 15) women in addition to the classical division according to menstrual cycle. Corresponding serum estradiol, progesterone and gonadotropin levels were measured, and the degree of ovarian stromal hyperplasia was analyzed. RESULTS: The levels of all steroid hormones were higher in the ovarian vein than in the periphery. A significant positive correlation was found between age and ovarian vein testosterone levels (r = 0.3, P = 0.01). In premenopausal women, it was 1.5 nmol/l (median; range 0.78-6.0), in perimenopausal women 2.2 nmol/l (range 0.9-13.6), and 2.5 nmol/l (range 0.6-26.6) in postmenopause, respectively. Peripheral testosterone level did not increase with age. Ovarian stromal hyperplasia was significantly associated with increased testosterone secretion (P = 0.009). CONCLUSION: The ovary seems to increase the secretion of testosterone into circulation during the menopausal transition period, as the highest levels were measured in postmenopausal women. High testosterone levels in the ovarian vein, however, were not reflected in the peripheral venous blood.

Inhibin A and B in peri- and postmenopause.

OBJECTIVE: The aim of the study was to investigate the origin of inhibin A and B during the last years of the reproductive age and after menopause by measuring their levels in the ovarian and peripheral venous blood. METHODS: The study population consisted of 43 women, aged 42-69 years (mean 50), who underwent hysterectomy with ovarian removal for a benign disease. A total of 24 of them were in follicular phase, 11 in luteal phase, and eight were postmenopausal. Peripheral and ovarian venous blood was collected for measurement of inhibin A and B. In addition, sex steroid hormone and gonadotropin levels were measured. RESULTS: Ovarian venous inhibin B correlated significantly with ovarian estradiol secretion (r = 0.5, P = 0.001). The levels of inhibin B were significantly higher in the ovarian vein than in the peripheral vein (P = 0.006). The highest inhibin B concentrations were detected in the mid-proliferative (mid-follicular) phase (median 31.6 pg/ml range 25.9-47.9). In postmenopausal women, inhibin B was not detectable. No correlation between FSH and ovarian inhibin B was found. Inhibin A rose rapidly in late proliferative (late follicular) phase (median 28.5, range < 2-51.8) and dominated in the circulation throughout the luteal phase (median 20.9, range 8.8-60). For inhibin A, no concentration gradient existed between the ovarian and peripheral vein. Unlike inhibin B, inhibin A was detectable in ovarian and peripheral blood in postmenopausal women. A significant negative correlation between ovarian and peripheral inhibin A and FSH was found (r = -0.386, P = 0.015; r = -0.345, P = 0.034, respectively). CONCLUSION: Inhibin B correlates with ovarian estradiol secretion and seems to reflect follicular function. Inhibin A dominates in circulation during the luteal phase but is detectable at low concentrations both in follicular phase and even in postmenopause. Our findings suggest that inhibin A may play a role in FSH suppression in the female reproduction. In addition to the ovary, there may be extragondal source(s) of inhibin A.

Helicobacter pylori: optimum diagnosis and test of cure.

The fact that about 50% of the world's population is infected with Helicobacter (H.) pylori and the important role that this bacterium plays in public health have been important incentives in the search for accurate diagnostic methods. A large number of invasive and non-invasive methods have been used to diagnose H. pylori infection. Each method has its advantages and disadvantages and each practitioner should choose the best diagnostic method according to the facilities available. Non-invasive tests for the diagnosis of H. pylori infection are largely used in clinical practice and in management of patients with gastroduodenal disease. Serology is the most widespread test but its use is not advised in the post-treatment follow-up. The Urea Breath Test is a simple, safe and highly accurate method ideal for evaluating the short-term follow-up of H. pylori eradication after therapy.

Is potential to produce inhibins related to prognosis in ovarian granulosa cell tumors?

OBJECTIVE: The prognosis of ovarian granulosa cell tumors is difficult to predict by conventional histological methods. STUDY DESIGN: The tumors of 30 patients operated on for a granulosa cell tumor were retrospectively studied for the expression of the inhibin alpha-subunit. The immunohistochemical staining results were correlated to the FIGO stage of the tumor and the prognosis of the patients. RESULTS: Twenty-six (87%) of the ovarian granulosa cell tumors stained positively for the inhibin alpha-subunit. All FIGO stage I and II tumors expressed inhibin alpha-subunit. All FIGO stage I and II tumors expressed inhibin, whereas the majority of stages III and IV did not (p=0.001, chi2-test). The survival of the patients with inhibin immunopositive tumors was significantly longer (median 183 months, SE 41, p=0.000, log rank test) than that of patients without inhibin expression (median 2.5 months, SE 5.25). CONCLUSIONS: Patients with ovarian granulosa cell tumors with a potential to produce the inhibin alpha-subunit may have a more favorable prognosis than those with inhibin immunonegative tumors.

Endoscopic surveillance in Barrett's esophagus.

Barrett's esophagus (BE), a complication of chronic gastroesophageal reflux disease (GORD), is a condition that is premalignant for adenocarcinoma of the esophagus and esophagogastric junction. Esophageal adenocarcinoma, once an uncommon entity, has been growing rapidly in incidence over the last two decades in several parts of the world. Barrett's esophagus is a change in the esophageal epithelium of any length that can be recognized at endoscopy and is confirmed to have intestinal metaplasia by biopsy (American College of Gastroenterology guidelines). Because of its premalignant nature, it is recommended that patients with BE undergo regular endoscopic surveillance. The recommendation for endoscopic surveillance is based on unproved and controversial assumptions including: 1) the assumption that Barrett's esophagus adversely influences survival; 2) the assumption that endoscopic surveillance can reliably detect early, curable neoplasia in the columnar lined esophagus. Moreover, the low incidence of adenocarcinoma (reported cancer incidence rates in prospective studies on BE range between 0.5% and 1.9%) is used to support an approach of not surveying patients with Barrett's esophagus. Despite these not convincing data, endoscopic surveillance is considered ''reasonable'' and ''desirable'' by the gastroenterological associations and consensus meetings. Endoscopic surveillance for cancer in Barrett's esophagus (BE) is performed primarily to seek dysplasia, to prevent the progression to invasive malignancy; however, one of the limitations of using dysplasia is a lack of understanding of its natural history. The efficacy of endoscopic surveillance for Barrett's esophagus is likely to remain unclear for a long time. The American College of Gastroenterology has recommended the following practice guidelines: a) for patients with no dysplasia, surveillance endoscopy is recommended at an interval of every 2 to 3 years; b) for patients with low grade dysplasia, surveillance endoscopy every 6 months for the first year is recommended, followed by yearly endoscopy if the dysplasia has not progressed in severity; c) for patients with high grade dysplasia, two alternatives are proposed after the diagnosis has been confirmed by an expert gastrointestinal pathologist. One alternative is intensive endoscopic surveillance until intramucosal cancer is detected at an interval of every 3-6 months. The other alternative is esophageal resection. In the situation of indeterminate dysplasia, whereas the pathologist can not come to definite diagnosis, control biopsies are proposed after 2 months of adequate acid suppression by means of proton pump inhibition. In all cases, the technique of random, four quadrant biopsies taken every 2 cm in the columnar-lined esophagus for standard histologic evaluation is recommended. Any grossly abnormal areas may be biopsied too. One can expect however that during the next future these protocol will change considering new data on dysplasia detection (biochemical markers, flow cytometry), new techniques to identify dysplasia (chromoendoscopy, endosonography, coherence optical tomography, fluorescence techniques) and development of better ablative techniques. At present a marker other than dysplasia identifying a high risk group for cancer on which to focus endoscopic surveillance has not yet been established.

Absent SEP during therapeutic hypothermia did not reappear after re-warming in comatose patients following cardiac arrest.

BACKGROUND: Early prediction of neurological outcome for patients resuscitated from cardiac arrest (CA) is a challenging task. Therapeutic hypothermia (TH) has been shown to improve neurological outcome after CA. Two recent studies indicated that somatosensory evoked potentials (SEP) recorded during TH retains high prediction value for poor neurological outcome. It remains unclear whether TH can influence the recovery of bilaterally absent (BA) N20 after re-warming. The primary endpoint of the present study was to evaluate if patients with BA SEPs during TH can recover cortical responses after re-warming. The secondary endpoint was to evaluate whether BA SEPs recorded during TH retains its prediction value for poor neurological outcome as in normothermic patients. METHODS: A single centre prospective cohort study including comatose adults resuscitated from in/out-of-hospital CA treated with TH. SEPs were recorded during TH (6-24 hours after CA) and after re-warming in those patients who remained comatose. Neurological outcome was assessed 6 months after CA using the Glasgow Outcome Scale. RESULTS: Sixty patients were included. In patients with preserved SEP, no significant differences were found between N20 mean amplitude during TH and after re-warming. During TH, 24 patients showed bilaterally absent N20 but none of these recovered cortical responses after re-warming. All patients with absent SEPs during TH did not recover consciousness. CONCLUSIONS: In a single centre cohort of comatose CA patients, our results showed that all patients with absent SEPs during early recording (6-24 hours) during TH showed bilaterally absent SEPs after re-warming. As a secondary result we confirmed previous data that BA SEPs during TH retains its prognostic value for poor neurological outcome, as in normothermic patients.

Transient post-traumatic locked-in syndrome: a case report and a literature review.

INTRODUCTION: Post-traumatic locked-in syndrome may be particularly difficult to recognize, especially when it follows a state of coma and presents the clinical feature of a "total" locked-in syndrome. PATIENT AND METHODS: A 56-year-old male with a closed head injury was admitted in intensive care unit (ICU) with GCS=4 (V1, M2, E1). Computed tomography (CT) scan disclosed a limited subarachnoid haemorrhage in the sylvian region without any brain oedema or ventricular shift. The GCS did not change until day 6. At the same time EEG showed a reactivity to acoustic stimuli consisting in the paradoxical appearance of a posterior rhythm in alpha range (10-12c/s), blocked by passive eye opening. Early cortical components (N20-P25) of somatosensory evoked potentials were normal on both hemispheres; middle components were also clearly evident. Magnetic resonance imaging of the brain showed both diffuse and midbrain axonal injuries, particularly in a strategic lesion involving both cerebral peduncles. Event related potentials showed N2 and P3 components to stimulation by rare tones. CONCLUSIONS: A comprehensive multimodal neurophysiological approach, using the more informative tests and the proper time of recording, should be included in protocols for patients with severe head trauma, in order to establish the actual patient's clinical state and to avoid that a locked-in syndrome state be mistaken for prolonged coma, vegetative state, minimally conscious state or akinetic mutism. Neurophysiological evaluation before discharge from ICU can be a baseline evaluation useful for the follow-up of low-responsive patients in the neuro-rehabilitation unit.

Continuous EEG-SEP monitoring in severe brain injury.

AIMS: To monitor acute brain injury in the neurological intensive care unit (NICU), we used EEG and somatosensory evoked potentials (SEP) in combination to achieve more accuracy in detecting brain function deterioration. METHODS: Sixty-eight patients (head trauma and intracranial hemorrhage; GCS<9) were monitored with continuous EEG-SEP and intracranial pressure monitoring (ICP). RESULTS: Fifty-five patients were considered "stable" or improving, considering the GCS and CT scan: in this group, SEP didn't show significant changes. Thirteen patients showed neurological deteriorations and, in all patients, cortical SEP showed significant alterations (amplitude decrease>50% often till complete disappearance). SEP deterioration anticipated ICP increase in 30%, was contemporary in 38%, and followed ICP increase in 23%. Considering SEP and ICP in relation to clinical course, all patients but one with ICP less than 20 mmHg were stable, while the three patients with ICP greater than 40 mmHg all died. Among the 26 patients with ICP of 20-40 mmHg, 17 were stable, while nine showed clinical and neurophysiological deterioration. Thus, there is a range of ICP values (20-40 mmHg) were ICP is scarcely indicative of clinical deterioration, rather it is the SEP changes that identify brain function deterioration. Therefore, SEP have a twofold interest with respect to ICP: their changes can precede an ICP increase and they can constitute a complementary tool to interpret ICP trends. It has been very important to associate SEP and EEG: about 60% of our patients were deeply sedated and, because of their relative insensitivity to anesthetics, only SEP allowed us to monitor brain damage evolution when EEG was scarcely valuable. CONCLUSIONS: We observed 3% of nonconvulsive status epilepticus compared to 18% of neurological deterioration. If the aim of neurophysiological monitoring is to "detect and protect", it may not be limited to detecting seizures, rather it should be able to identify brain deterioration, so we propose the combined monitoring of EEG with SEP.