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D Gastfriend

Publications and source records attributed to D Gastfriend.

4 recordsLinked to original sources
PubMed1998

Cocaine decreases cortical cerebral blood flow but does not obscure regional activation in functional magnetic resonance imaging in human subjects.

The authors used functional magnetic resonance imaging (fMRI) to determine whether acute intravenous (i.v.) cocaine use would change global cerebral blood flow (CBF) or visual stimulation-induced functional activation. They used flow-sensitive alternating inversion recovery (FAIR) scan sequences to measure CBF and blood oxygen level-dependent (BOLD) sensitive T2* scan sequences during visual stimulation to measure neuronal activation before and after cocaine and saline infusions. Cocaine (0.6 mg/kg i.v. over 30 seconds) increased heart rate and mean blood pressure and decreased end tidal carbon dioxide (CO2). All measures returned to baseline by 2 hours, the interinfusion interval, and were unchanged by saline. Flow-sensitive alternating inversion recovery imaging demonstrated that cortical gray matter CBF was unchanged after saline infusion (-2.4 +/- 6.5%) but decreased (-14.1 +/- 8.5%) after cocaine infusion (n = 8, P < 0.01). No decreases were detected in white matter, nor were changes found comparing BOLD signal intensity in cortical gray matter immediately before cocaine infusion with that measured 10 minutes after infusion. Visual stimulation resulted in comparable BOLD signal increases in visual cortex in all conditions (before and after cocaine and saline infusion). Despite a small (14%) but significant decrease in global cortical gray matter CBF after acute cocaine infusion, specific regional increases in BOLD imaging, mediated by neurons, can be measured reliably.

Adult↗
PubMedDate not supplied

Comorbidity, smoking behavior and treatment outcome.

BACKGROUND: A sizeable sector of the population continues to smoke cigarettes despite our efforts to prevent and treat this addiction. We explored the relationships between lifetime comorbidity, psychiatric symptomatology, smoking behavior and treatment outcome to better understand vulnerability to smoking and treatment response. METHODS: One hundred and twenty smokers at two sites were enrolled in a multicenter, double-blind, randomized, 10-week smoking cessation trial with fluoxetine and behavioral treatment. The Structured Clinical Interview for DSM-III-R and Hamilton Depression Rating Scale were administered prior to treatment initiation. Self-report measures were used to assess psychiatric symptoms throughout treatment and during a 6-month follow-up period. RESULTS: Overall 62.3% of our sample were diagnosed with a lifetime mood, anxiety or substance use disorder despite stringent study exclusion criteria. Lifetime comorbidity was shown to be related to higher smoking rates and nicotine dependence, depressed mood and greater self-report of anxiety and stress. Lifetime comorbidity, however, alone or in combination with treatment condition, failed to predict treatment outcome (at posttreatment or follow-up). Baseline depression scores (Beck Depression Inventory, BDI) were related to treatment outcome only for smokers without a positive history of any psychiatric disorder or depression, with lower BDI scores more frequent in those who were abstinent. CONCLUSIONS: High prevalence rates of lifetime psychiatric illness and substance use disorders are reported for chronic smokers. Subsyndromal psychiatric symptoms may play a role in smoking behavior in combination with diagnosable disorders. Clinicians need to carefully assess both psychiatric diagnoses and symptoms in chronic smokers to optimize patient-treatment matching.

Adolescent↗