The incidence of T2-weighted MR imaging signal abnormalities in the brain of cocaine-dependent patients is age-related and region-specific.

BACKGROUND AND PURPOSE: Cocaine and its metabolites can produce vasospasm, and cocaine-dependent patients are at increased risk for stroke. Based on previous case reports, we hypothesized that the incidence of hyperintense brain lesions observed on T2-weighted MR images would also be increased in asymptomatic cocaine-dependent individuals. METHODS: Sixty-two male "crack" (smoked) cocaine-dependent participants ranging in age from 25 to 66 years were compared with 116 normal male control participants ranging in age from 25 to 80 years. Those with histories of neurologic symptoms or illnesses were excluded. The severity of hyperintense lesions was rated on a 0- to 3-point scale, and ratings of 3 were used in the data analysis as an indicator of a probable pathologic process. Three regions were separately rated: the cerebral white matter, insular subcortex white matter, and subcortical gray matter (basal ganglia and thalamus region). RESULTS: Significantly increased risk of severe lesions was observed in the two white matter regions of the cocaine-dependent group (odds ratio of 16.7 and 20.3) but not in the subcortial gray matter region (odds ratio of 1.4). In the insula subcortex white matter, the risk of lesions increased with age in the cocaine-dependant sample, but remained essentially absent among normal controls through the age of 80 years. In the cerebral white matter, the relationship of age and risk of lesion among normal participants was similar in shape to that in cocaine-dependent participants, but equivalent risk was seen 20 years earlier among cocaine-dependent participants. CONCLUSIONS: Cocaine-dependent participants had a significantly increased age-related risk of white matter damage. The possible clinical implications of this damage are discussed.

Blood pressure response to the "second cup of coffee".

Twenty young male coffee-drinkers consumed 150 mg of caffeine in decaffeinated coffee three times a day for 8 days. On days 3, 4, 7, and 8, caffeine or a placebo was administered in the laboratory at 11 A.M., 8 A.M., 11 A.M., and 8 A.M., respectively, in a randomized double-blind crossover design. There was a blood pressure increase relative to the placebo 45 min after taking caffeine at 8 A.M. (5.8/6.5 mm Hg). An increase of 2.4/5.2 mm Hg was seen with the second cup of coffee at 11 A.M. The lower the subject's pre-coffee serum caffeine level, the higher the systolic response, both at 8 A.M. (r = -0.60) and at 11 A.M. (r = -0.62). Because of the pressor effect resulting from habitual caffeine intake, the adverse implications of caffeine use should be considered.

Home relaxation techniques for essential hypertension.

A 10-week relaxation treatment focused on home practice and self-monitoring of blood pressure for the purpose of lowering blood pressure in patients with essential hypertension. Comparisons were made among relaxation (n = 13), relaxation in combination with electromyographic biofeedback (n = 14), and a control condition in which patients simply monitored their blood pressure (n = 14). These three groups of patients, all of which received antihypertensive medication, were compared with a fourth group that practiced relaxation without drug therapy (n = 17). Relaxation and relaxation/biofeedback were equally effective in reducing blood pressure recorded at home in the morning and evening and produced greater decreases than in the control group. Relaxation without drugs, although somewhat more effective than self-monitoring, did not reduce blood pressure as much as the two conditions in which medication was combined with relaxation. Although reductions over the course of treatment were noted in blood pressure recorded in the laboratory, the four treatment conditions did not differ significantly from one another.