In an analysis of a large cohort of subjects with IBD, we found a significant association between symptoms of depression or anxiety and clinical recurrence. Patients with IBD should therefore be screened for clinically relevant levels of depression and anxiety and referred to psychologists or psychiatrists for further evaluation and treatment.

It is widely agreed that after two or more seizures patients should be given antiepileptic treatment, but there is still controversy about the treatment of patients after a first unprovoked seizure. In a multicenter, randomized, open trial, patients with a first tonic-clonic seizure were randomized to immediate treatment (carbamazepine, phenytoin, phenobarbital, or sodium valproate) or to treatment only after another seizure. Fifty-two (24%) of the 215 patients randomized to immediate treatment and 85 (42%) of the 204 randomized to delayed treatment experienced seizure recurrence during follow-up. Age, acute treatment of the seizure with benzodiazepines, remote etiologic factors, and EEG abnormalities were significant predictors of relapse. Of the immediately treated patients, 87% had no seizures for a year and 68% had no seizures for 2 years, whereas only slightly fewer initially untreated patients (83% and 60%) achieved these endpoints. Patients treated after the first seizure and those treated after seizure relapse had the same time-dependent probability of achieving 1 and 2 seizure-free years. None of the variables that were prognostic predictors of relapse was significantly associated with the probability of having 1 or 2 years of seizure control. Anticonvulsants in patients presenting a first tonic-clonic seizure reduce the risk of relapse; however, 50% of patients who are not treated will never experience a second seizure. Moreover, the probability of long-term remission is not influenced by treatment of the first seizure.

To test the hypothesis that Helicobacter pylon1 infection is associated with a decreased intragastric acidity during omeprazole therapy, ambulatory 24 hour dual point gastric pH recordings were performed in 18 H pyloni positive and 14 H pylori negative subjects. There was a four to six week washout period between the two pH recordings made in each subject after one week courses of placebo or omeprazole, 20 mg daily. During placebo, median 24 hour pH values were not different in the corpus (H pylori positive=1.5, negative=1-4; p=0*9) or antrum (H pyloni positive= 13, negative= 12; p=0 1). However, during omeprazole treatment, median 24 hour pH values were higher in H pylori positive subjects, both in the corpus (H pylori positive=5 5, negative=4*0; p=0.001) and antrum (H pylorn positive=5.5, negative=3.5; p=0.0004). During placebo treatment, the only difference between the two groups was a higher later nocturnal pH in the antrum in the H pylorn positive group. During omeprazole treatment, gastric pH was higher both in the corpus and in the antrum in the H pylon positive group for all periods, except for mealtime in the corpus. These data indicate that omeprazole produces a greater decrease in gastric acidity in subjects with H pylon infection than in those who are H pylon negative. It is not, however, known whether there is a causal relationship between H pylorn infection and increased omeprazole efficacy. (Gut 1995; 36: 539-543) Keywords: Acid inhibition, Helicobacter pylori, omeprazole, intragastric pH-metry.Omeprazole has been shown to have both direct1 and indirect23 effects on Helicobacter pylori, but it is not known whether infection with the organism may itself influence gastric acidity during omeprazole therapy. It has been reported that during treatment with omeprazole, the intragastric pH is higher in patients with duodenal ulceration than in healthy controls.4 5 It is unclear whether this reduction in gastric acidity is observable in all subjects with H pylori infection, or whether it is confined to a subset of patients who develop peptic ulceration. If the increased susceptibility to omeprazole is related solely to Hpylori infection then Hpyloni negative subjects and H pylori positive subjects without ulceration should show different degrees of acid suppression in response to an equal dose of omeprazole.To test the hypothesis that Hpylori infection is associated with decreased intragastric acidity during treatment with omeprazole, we have conducted gastric pH-metry in H pylori positive individuals and compared the pH data with those obtained previously in 14 H pylori negative individuals. Methods SUBJECTSFourteen H pylon negative healthy subjects (seven men and seven women, age range: 22-46 years) and 18 H pylori positive subjects (1 1 men and seven women, age range: 22-45 years) were studied. Students and employees of a university hospital who had volunteered for an H pylori screening programme were also invited to participate in the present study. H pylori status was determined using the ...

We studied the seizure and polygraphic patterns of 18 patients with Angelman's syndrome. All patients showed movement problems. Eleven patients were also reported to have long-lasting periods of jerky movements. The polygraphic recording showed a myoclonic status epilepticus in nine of them. Seven patients had partial seizures with eye deviation and vomiting, similar to those of childhood occipital epilepsies. These seizures and electroencephalographic patterns suggest that Angelman's syndrome occurs in most of the patients as a nonprogressive, age-dependent myoclonic encephalopathy with a prominent occipital involvement. These findings indicate that, whereas ataxia is a constant symptom in Angelman's syndrome, the occurrence of a transient myoclonic status epilepticus may account for the recurrence of different abnormal movements, namely the jerky ones.

Previous studies have suggested that profound inhibition of gastric acid secretion may increase exposure to potentially carcinogenic N-nitroso compounds. The 42 (19-194) ml).The concentration of N-nitroso compounds was 0-13 (0-1-0) ptmol/l after two weeks of omeprazole, which was not significantly different from that seen with placebo (0-15 (0-0.61) tmol/l). There was also no increase in the concentrations of nitrates or nitrites. It is concluded that omeprazole (20 mg once daily) for two weeks in healthy volunteers is associated with gastric bacterial proliferation but does not increase concentrations of N-nitroso compounds. (Gut 1994; 35: 455-460) Omeprazole has been established as an effective treatment for peptic ulceration and reflux oesophagitis, for periods of up to five years.' 5 There are still concerns regarding the possible risks of prolonged gastric acid suppression.6-9 Prominent among these are uncertainties of adverse effects consequent on bacterial proliferation and colonisation of the upper gastrointestinal tract.