Research on the brain
Any hopes for therapy after major brain trauma depend ultimately on the capacity of the central nervous system to encode and integrate into its working systems a changed circuit. Professor Mike Calford has dedicated many years to attempt to understand why.
Professor Calford's experiments, which began at the University of Queensland around 1984, were based on the need to understand that capacity for change and then to develop the tools necessary to manipulate that capacity. The approach was to develop appropriate animal models that allow this capacity to be studied in the intact animal.
About 30 years ago the adult brain was thought of as a structurally fixed organ, incapable of major recovery from injury, disease or the effects of ageing. Professor Calford's group was one of the first to demonstrate that this is not the case. By studying simple models of brain injury, using the spinal- and brain-representations of the tactile (and later visual and auditory) system of animals as models, Professor Calford helped overthrow prevailing dogma by revealing the physiological time-course of this plasticity.
Later work showed the limitations that the mechanisms of adult brain plasticity place upon expectations for change and recovery from trauma.
Whereas the initial focus was basic research, there has nonetheless been the expectation that revealing fundamental aspects of the brains inherent capacity for plasticity would have significant implications for clinical practice and educational theory.
This potential has indeed been realised, with Professor Calford's discoveries having a major influence on the direction of clinical research. Specifically, the knowledge of neuronal plasticity gained through this work has been used to examine possible therapies for ischemic stroke. For example, Professor Calford's work showing that activity in primary somatosensory cortex exerts an inhibitory influence on its contralateral counterpart which can be interrupted by a reduction of peripheral input (Science 249: 805-807; Cerebral Cortex 6:196-206), is the primary impetus for a series of investigations into changes in tactile sensitivity contingent upon anaesthesia or nerve damage to the contralateral arm in humans. This work is being conducted at the NIH laboratories in Bethesda by Leonardo Cohen and colleagues and is aimed at improving stroke recovery manipulation therapies (NIH notification of the clinical trial - NCT00056706).
Recent and current work is directly influenced by clinical questions being applied back to animal models for testing, for example, examining the basis, and optimal timing, of acute hypothermia treatment for ischaemic stroke; and models of environmental enrichment for long term rehabilitation.