Because of the epidemiological transition, the global burden of illness has changed. Several factors have contributed to this change, including improvements in maternal and child health, increasing age of populations, and newly recognized disorders of the nervous system. It is now evident that neurologic disorders have emerged as priority health problems worldwide. This is reflected in the Global Burden of Disease Study, jointly published by the World Health Organization and other groups. The proportionate share of the total global burden of disease resulting from neuropsychiatric disorders is projected to rise to 14.7% by 2020. Although neurologic and psychiatric disorders comprise only 1.4% of all deaths, they account for a remarkable 28% of all years of life lived with a disability. This study provides compelling evidence that one cannot assess the neurologic health status of a population by examining mortality statistics alone. Health ministries worldwide must prioritize neurologic disorders, and neurologists must be prepared to provide care for increased numbers of people individually and in population groups.

SUMMARY Thirteen consultant neurologists working in ten different towns or cities in the United Kingdom were asked to log all their encounters with patients in 1 week. The median number of encounters was 79 (range 33-144). Forty-one per cent were new patients; 85% of all new patient encounters were with National Health Service patients. In more than four-fifths ofall encounters, the neurologist felt that the consultation was ajustified use ofhis experience. Consultations for headache/ migraine and epilepsy together accounted for over a quarter of all encounters.

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SUMMARY 1. The uncoupling of oxidative phosphorylation of liver mitochondria by bilirubin does not occur in the presence of equimolar quantities of human serum albumin. With brain mitochondria, however, albumin was not protective. 2. A similar protective effect of albumin for liver, but not for brain, mitochondria was observed in studies of the effects of bilirubin on the 32Pi‐ATP exchange reaction. 3. The latent ATPase of fresh brain mitochondria is activated by Mg2+ but only slightly by DNP. Bilirubin increased the Mg2+ stimulated ATPase activity in liver mitochondria but depressed this activity in brain mitochondria. These effects were uninfluenced by protein binding. 4. Isotope studies with [14C]bilirubin demonstrated that the affinity of brain mitochondria for albumin‐bound bilirubin is not greater than that of liver mitochondria. 5. The greater toxicity of protein‐bound bilirubin for brain mitochondria than for liver mitochondria might be related to the greater lipid content of brain mitochondria.

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