Dipyridamole dilates large cerebral arteries concomitant to headache induction in healthy subjects.

Dipyridamole is used for secondary prophylaxis in ischemic stroke and as a vasodilator agent in myocardial scintigraphy. An important side effect to administering dipyridamole is headache. The aim of the current study was to investigate the effects of dipyridamole on cerebral blood flow, large artery diameter, and headache induction. Twelve healthy subjects were included in this single-blind placebo-controlled study in which placebo (0.9% NaCl) and dipyridamole 0.142 mg/kg x min were administered intravenously over 4 minutes 1 hour apart. Blood flow velocity in the middle cerebral artery (Vmax) was recorded by transcranial Doppler and regional cerebral blood flow in the middle cerebral artery (rCBFmca) was measured using single photon emission computed tomography and 133Xenon-inhalation. Blood pressure, heart rate, and pCO2 were measured repeatedly. Headache response was scored every 10 minutes on a verbal scale from 0 to 10 (10 = worst). Dipyridamole caused a decrease in pCO2 (P < 0.001). pCO2 corrected rCBFmca was 41.7 +/- 6.9 mL/100 g x min after placebo versus 41.2 +/- 6.9 after dipyridamole (P > or = 0.05). pCO2 corrected Vmca decreased 8.4% +/- 11.7 (P < 0.001) after dipyridamole, indicating a mean 5.6% +/- 6.7 (P = 0.005) relative increase of the arterial diameter. After dipyridamole the median peak headache score was 2 (range 0 to 7) compared with 0 (range 0 to 3) after placebo (P = 0.02). Dilatation of the middle cerebral artery outlasted the headache response. In conclusion, dipyridamole causes a modest pCO2 independent dilatation of the MCA, which is time-linked to the onset, but not to the cessation, of headache.

Schizoaffective disorder-- the reliability of its clinical diagnostic use.

OBJECTIVE: Patients with psychoses often suffer from affective symptoms. The originally broad concept of schizoaffective disorder (SAD) has been significantly narrowed, transformed into a convoluted set of criteria both in the ICD-10 and DSM-IV. We examined the reliability of the clinical use of this diagnosis in university settings. METHOD: All patients discharged from two university hospitals in Copenhagen in year 2002 with a diagnosis of ICD-10 SAD (n = 59) were re-evaluated using the Operational Criteria (OPCRIT) checklist expanded by additional items and applied to hospital chart material. Diagnoses were allocated by OPCRIT algorithm and by consensus of two psychiatrists. RESULTS: No patients fulfilled the SAD lifetime diagnosis according to DSM-IV criteria and the raters diagnosed only six patients as possible ICD-10 SAD. CONCLUSION: A moratorium on the clinical use of the SAD diagnosis is suggested.

Effects of the non-selective phosphodiesterase inhibitor pentoxifylline on regional cerebral blood flow and large arteries in healthy subjects.

The vasodilating properties of the non-selective phosphodiesterase (PDE) inhibitor pentoxifylline were evaluated. Pentoxifylline has been reported to increase cerebral blood flow (CBF) and improve recovery rate of stroke patients. Whether these results are due to a dilating effect on arteries or to other mechanisms is not clear. In the present double-blind crossover study, 10 healthy subjects received pentoxifylline 300 mg or placebo intravenously on separate days. Blood flow velocity in the middle cerebral artery (V(mca)) was recorded by transcranial Doppler and rCBF was measured using (133)Xenon-inhalation SPECT. High-frequency ultrasound was used for measurements of temporal and radial artery diameter. Cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) concentrations were assessed in plasma. Except for increased heart rate (P < 0.05), systolic blood pressure (P < 0.05) and plasma cAMP (P < 0.001), no significant differences in CBF, rCBF(mca) or plasma cGMP were seen between placebo and pentoxifylline infusion. During pentoxifylline infusion, V(mca) decreased 7.2% (SD 12.0; P < 0.05) and temporal artery diameter increased 9.0% (SD 7.0; P < 0.001), suggesting minor dilatation of the large arteries. However, this change was not significantly different from placebo. In conclusion, pentoxifylline 300 mg had no effect on rCBF. A possible minor dilatation of the middle cerebral artery and the temporal artery cannot be excluded. Any potential clinical effect of pentoxifylline is most likely mediated through non-vascular mechanisms.