Cognitive Behavioral Therapy for the Management of Multiple Sclerosis-Related Pain: A Randomized Clinical Trial.

BACKGROUND: Pain is a common and often debilitating symptom in persons with multiple sclerosis (MS). Besides interfering with daily functioning, pain in MS is associated with higher levels of depression and anxiety. Although cognitive behavioral therapy (CBT) for pain has been found to be an effective treatment in other populations, there has been a dearth of research in persons with MS. METHODS: Persons with MS with at least moderate pain severity (N = 20) were randomly assigned to one of two groups: CBT plus standard care or MS-related education plus standard care, each of which met for 12 sessions. Changes in pain severity, pain interference, and depressive symptom severity from baseline to 15-week follow-up were assessed using a 2×2 factorial design. Participants also rated their satisfaction with their treatment and accomplishment of personally meaningful behavioral goals. RESULTS: Both treatment groups rated their treatment satisfaction as very high and their behavioral goals as largely met, although only the CBT plus standard care group's mean goal accomplishment ratings represented significant improvement. Although there were no significant differences between groups after treatment on the three primary outcomes, there was an overall improvement over time for pain severity, pain interference, and depressive symptom severity. CONCLUSIONS: Cognitive behavioral therapy or education-based programs may be helpful adjunctive treatments for persons with MS experiencing pain.

Neuropsychological impairment in patients with schizophrenia and evidence of hyponatremia and polydipsia.

Patients with schizophrenia and water imbalance may represent a subset of patients with distinct pathophysiological abnormalities and susceptibility to cognitive impairment. Specifically, patients with polydipsia and hyponatremia have been shown to have smaller anterior hippocampal volumes, which are also associated with various impairments in neuroendocrine function. To determine whether abnormalities in patients with water imbalance extend to the cognitive realm, the present study evaluated neuropsychological functioning in three groups of patients with schizophrenia: polydipsic hyponatremic, polydipsic normonatremic, and nonpolydipsic normonatremic. Participants were administered cognitive tests assessing intelligence, attention, learning/memory (verbal, nonverbal, emotional), and facial discrimination. Hyponatremic patients showed poorer overall neuropsychological functioning relative to all other patients, and polydipsic normonatremic patients performed intermediate to the other two groups. Results indicate that patients with schizophrenia and polydipsia, and particularly those with hyponatremia, show prominent cognitive deficits relative to patients without water imbalance. The clinical, neuroendocrine, and cognitive abnormalities in these patients may arise from pathology within the anterior hippocampus and associated prefrontal/limbic brain regions.

Noradrenergic antagonism of the P13 and N40 components of the rat auditory evoked potential.

RATIONALE: Two rat auditory evoked potential (AEP) components P13 and N40 are suggested as analogues to the human P50, which has abnormal suppression properties in schizophrenia. However, P50 likely reflects neural activity from several different brain areas. Studies examining each of these components in the rat model have proposed circuitry that involves alpha2 norepinephrine (NE) receptors, and different disruption effects are predicted depending on whether effects are presynaptic or postsynaptic. OBJECTIVES: The aim of this paper is to test differential effects of NE antagonism on disruption of normal P13 and N40 expression. MATERIALS AND METHODS: AEPs were recorded simultaneously in alert, freely moving rats using the alpha2 antagonist yohimbine. Amplitudes of P13 and N40 elicited by 500-ms interstimulus interval click pairs were measured after administration of a placebo and three doses of the yohimbine. RESULTS: A high dose of yohimbine yielded smaller P13 amplitudes to both clicks, consistent with presynaptic action. However, a moderate yohimbine dose yielded increased P13 amplitudes to both clicks. For N40, a moderate dose of yohimbine yielded increased amplitudes to the second stimulus, and a high dose restored normal suppression, which is consistent with previously reported findings. CONCLUSIONS: This study demonstrated that noradrenergic activity differentially affects P13 and N40 components. As P13 and N40 are each models of human P50, these findings highlight the complex circuitry that likely underlies P50. An appreciation for these complexities is critical for understanding the mechanisms of the P50 suppression deficit in schizophrenia, which may be influenced by both trait and state factors.