Reductions in regional cerebral perfusion, particularly in the posterior temporo-parietal lobes, are well recognized in Alzheimer's disease. We set out to correlate perfusion changes, using (99m)Tc-HMPAO single photon emission tomography (SPET), with the pathological stage of Alzheimer's disease. The 'Braak stage' of the distribution of neurofibrillary pathology in post-mortem brains was used to classify SPET scans taken in life from a mixed (dementia and control) elderly population into the entorhinal stage (n = 23 subjects), limbic stage (n = 30 subjects) and neocortical stage (n = 36 subjects) Alzheimer's disease pathology. The SPET scans were then registered to a common, standard Talaraich space, and single template scans produced for each pathological stage. Comparison of these templates revealed an evolution in the pattern of reduction in regional perfusion. Additional comparisons were performed using earlier SPET scans obtained 5 years before death. For comparisons between templates, a threshold of 10% perfusion change was chosen so as to be clinically relevant as well as statistically significant. Reduced perfusion appears between the entorhinal and limbic stages in the anterior medial temporal lobe, subcallosal area, posterior cingulate cortex, precuneus and possibly the supero-anterior aspects of the cerebellar hemispheres. Large posterior temporo-parietal perfusion defects then appear between the limbic and neocortical stages, before finally large frontal lobe perfusion defects. The time course of these perfusion defects appears relatively long, suggesting that perfusion changes may have scope to be a diagnostic aid in staging Alzheimer's disease in life. The reduction in anterior medial temporal lobe perfusion may have future relevance on modern high resolution SPET and PET systems and also perfusion-type MRI sequences.

A combination of medial temporal lobe atrophy, shown by computed tomography, and reduced blood flow in the parietotemporal cortex, shown by single photon emission tomography, was found in 86% (44151) of patients with a clinical

A controlled, prospective study comparing streptokinase and heparin treatment has been completed in 51 patients presenting with acute proximal venous thrombosis of less than 8 days' clinical duration. Patients were studied by means of pre-treatment, post-treatment, 3- and 12-monthly phlebography and pulmonary perfusion scanning and were followed up at 3-monthly intervals. Of the 26 patients randomized to receive streptokinase, therapy was stopped in 3 because of complications. Phlebography 5 days after starting treatment showed 80--100 per cent lysis in 17 of the 23 patients who completed the course of streptokinase. Two patients later developed partial rethrombosis. One patient developed an asymptomatic pulmonary embolus during treatment. During follow-up (mean 19 months) only 1 of the 17 patients with 80--100 per cent lysis developed postphlebitic symptoms, 3 patients died of unrelated causes and 1 patient was lost to follow-up. In patients randomized to heparin therapy no significant lysis was achieved in any of the 25 patients and only 2 of these patients were found to have asymptomatic legs on follow-up. Two patients in this group died and autopsy confirmed massive pulmonary embolus during treatment. These data suggest that streptokinase is superior to heparin in the treatment of acute proximal venous thrombosis of less than 1 week's clinical duration especially if the thrombus is largely non-occlusive. It must be stressed that in order to avoid the bleeding complications of thrombolytic therapy, streptokinase must not be used within 10 days of major surgery, or even longer after vascular, neurosurgical or eye operations.

Problems arise in distinguishing skeletal from cardiac muscle trauma on the basis of serum enzyme tests following severe muscle exercise. The contributions of cardiac and skeletal sources have been assessed in eleven marathon runners by measuring pre- and post-race serum levels of cardiac-specific myofibrillar troponin-I together with total creatine kinase, creatine kinase-MB isoenzyme, myoglobin, myofibrillar tropomyosin and C-reactive protein. Total creatine kinase, creatine kinase-MB isoenzyme, tropomyosin and myoglobin were significantly elevated above pre-race levels in all runners between 1 h and 128 h post-race. Neither mean cardiac troponin-I nor C-reactive protein was elevated post-race. Nine out of sixty-three samples fulfilled conventional positive criteria for cardiac muscle damage on the basis of combined creatine kinase and creatine kinase-MB isoenzyme levels. Six runners had one or more positive samples. No samples had levels above twice the upper normal limit for either cardiac troponin-I or C-reactive protein. Correlation analysis of levels in each sample indicated skeletal and not cardiac muscle as the source of raised serum protein.