Distribution of11 C–labelled morphine and pethidine after spinal administration to Rhesus monkey

The kinetics of 11C-labelled morphine and pethidine were studied by positron emission tomography (PET) at different levels of the spinal canal (C4, T4, T5, T6, L1 and L6). Studies were performed in the Rhesus monkey after intrathecal and extradural administration of the drugs at the lumbar level (L3-L4 or L4-L5, seven experiments). Radioactivity 100-300 times higher than with even distribution in the body was measured initially near the site of injection for both morphine and pethidine, irrespective of the route of administration. After injection of pethidine, high activity was observed at the L6 and L1 levels, whilst the radioactive uptake was lower at T6 (10-20% of those at lumbar level). Morphine-derived 11C-radioactivity showed more constant levels along the spinal canal, except at C4 where radioactivity was low. In CSF taken from the cervical level the peaks of radioactivity of the two drugs appeared 80-170 min after injection. The importance of different distribution routes was quantified in a pharmacokinetic compartment model, using the above results. The systemic distribution was extensive, irrespective of drug or route of administration. From the site of injection the systemic distribution was at least 60 times larger than the rostral distribution within the spinal canal.     

Gradient recalled echo MR imaging of the jugular foramen

Axial T1-weighted spin-echo MR images have not proved to be effective in identifying normal structures in the jugular foramen. By correlating cryomicrotomic sections and axial T1-weighted gradient recalled echo images, we identified the neural and vascular contents of the jugular foramen. Further work with gradient recalled echo images is needed to determine the signal characteristics of jugular foraminal lesions.     

Mechanical Wear of Pacemaker Lead Insulation. A Cause of Loss of Pacing

A pacemaker-treated patient is described in whom lead insulation defect caused sudden loss of capture. The defect was caused by mechanical wear of the posterior leaflet of the tricuspid valve and resulted in shunting of the pulse generator with a current drain exceeding the capacity of the pacemaker. In three further cases a similar explanation to sudden loss of pacing was highly suspected.