Tolerance for rectosigmoid distention in irritable bowel syndrome.

Two hypotheses were tested: (a) lowered tolerance for balloon distention of the rectosigmoid in patients with irritable bowel syndrome is caused by a psychological tendency to exaggerate the painfulness of any aversive stimulus, and (b) contractions elicited by balloon distention are responsible for pain reports. Tolerance for stepwise distention of a balloon in the rectosigmoid was compared with tolerance for holding one hand in ice water in 16 irritable bowel patients, 10 patients with functional bowel disorder who did not satisfy restrictive criteria for irritable bowel, 25 lactose malabsorbers, and 18 asymptomatic controls. Contractile activity was measured 5 cm above and 5 cm below the distending balloon. Psychometric tests were used to assess neuroticism, anxiety, and depression, and a standardized psychiatric interview was administered. Patients with irritable bowel syndrome had significantly lower tolerance for balloon distention but not ice water, and balloon tolerance was not correlated with neuroticism or other psychological traits measured. Rectosigmoid and rectal motility were also not related to tolerance for balloon distention. Both hypotheses were rejected. A peripheral mechanism such as altered receptor sensitivity may be the cause of distention pain in irritable bowel syndrome.

Behavioral treatment of intractable chest pain in a patient with vigorous achalasia.

Chest pain is a major symptom of patients diagnosed with esophageal motility abnormalities. Motility disorders of the esophagus are also associated with elevated scores on measures of somatic anxiety and depression. In spite of this relationship between psychological characteristics and esophageal motility disturbances, few attempts have been made to treat complaints of chest pain in patients with esophageal motility disorders using psychological methods. This report describes the successful use of a behavioral pain management program for the treatment of persistent chest pain in a patient diagnosed with vigorous achalasia who was previously treated with pneumatic dilatation and a long Heller myotomy. This is the first report on the use of psychotherapy in treating chest pain associated with vigorous achalasia, and suggests that, in the etiology and treatment of chest pain in patients with esophageal motility disturbances, psychological influences may be more important than has generally been recognized. No long-term relationship between esophageal motility disturbances and complaints of chest pain was found.

A double-blind investigation of the relationship between seizure activity and the sleep EEG following EEG biofeedback training.

The sleep EEGs of eight medically refractory epileptic patients were examined as part of a double-blind, ABA crossover study designed to determine the effectiveness of EEG biofeedback for the control of seizures. The patients were initially reinforced for one of three EEG criteria recorded from electrodes placed over sensorimotor cortex: (a) suppression of 3- to 7-Hz activity, (b) enhancement of 12- to 15-Hz activity, or (c) simultaneous suppression of 3- to 7-Hz and enhancement of 11- to 19-Hz activity. Reinforcement contingencies were reversed during the second or B phase, and then reinstated in their original form during the final A' phase. All-night polysomnographic recordings were obtained at the end of each conditioning phase and were subjected to both visual and computer-based power spectral analyses. Four of the patients showed changes in their nocturnal paroxysmal activity that were either partially or totally consistent with the ABA' contingencies of the study. The spectral data proved difficult to interpret, though two trends emerged from the analyses. Decreases in nocturnal 4- to 7-Hz activity were correlated with decreases in seizure activity, and increases in 8- to 11-Hz activity were correlated with decreases in seizure activity. These findings were shown to strengthen the hypothesis that EEG biofeedback may produce changes in the sleep EEG that are related to seizure incidence.

EEG operant conditioning in intractable epileptics.

Eight epileptic patients with mixed seizures refractory to medical control participated in a double-blind crossover study to determine the effectiveness of operant conditioning of the EEG as an anticonvulsant procedure. Baseline levels of seizures were recorded for four months prior to the beginning of treatment. Participants then received false (noncontingent) feedback for two months followed by an ABA-patterned training program lasting a total of ten months. Subjects were assigned to three treatment groups based on different schedules of EEG feedback. They were first trained (A1 phase) either to suppress slow activity (3 to 8 Hz), to enhance 12- to 15-Hz activity, or to simultaneously suppress 3- to 8-Hz and enhance 11- to 19-Hz activity. This was followed by a B phase, in which patients were trained to enhance slow activity (3 to 8 Hz). In the final phase (A2), the initial training contingencies were reinstated. Neuropsychological tests were performed before and after training, and changes in EEG activity as determined by Fast Fourier spectral analyses were analyzed. Five of eight patients experienced a decrease in their mean monthly seizure rate at the completion of feedback training as compared with their initial baseline level.