It was during this period he began to develop the then novel view that infectious disease is caused not directly by the invading pathogen, but by the host's innate immunity to it. The host-derived mediators of this response, such as TNF and IL-1, when produced excessively, were argued to generate disease through disrupting the normal homeostatic physiological roles of these cytokines. On returning to Australia he has continued to develop this idea of excessive production of these cytokines, particularly TNF, being central to pathogenesis of non-infectious as well as infectious diseases. Present interest focuses on a number of chronic brain diseases that may exhibit reduced cognition, behavioral changes, neuropathic pain and fatigue, including the encephalopathies such as post-stroke syndromes, post-cerebral malaria syndrome, Parkinson’s disease, cerebral palsy, traumatic brain injury and Alzheimer’s disease. He has focused on the concept of these and similar conditions have a fundamental similarity in their pathogenesis that is best regarded as manifestations of chronic cerebral inflammation. This is characterised by excess cerebral production of potentially pro-inflammatory cytokines that at low levels are essential components of normal cerebral physiology. A corollary is that specific anti-TNF agents such as etanercept, when administered appropriately, can lower cytokine levels and thus be usefully employed in the treatment of these conditions.