Neuromaging Diaschisis-Related Recovery
Functional imaging in a primate model provides insight into the distributed networks associated with changes in motor function. Autoradiography was performed on the macaque monkey after unilateral ablation of cortical areas 4 and 6 on the left. Partial recovery of the local cerebral metabolic rate for 14C-2-deoxygl ucose in a number of subcortical structures accompanied partial motor recovery.341 At 1 week, when the animal was hemiplegic, hypometabolism was found in the ipsilateral thalamus and the basal ganglia, structures that receive direct and indirect input from the motor cortex. Activity was diminished as well in the contralateral cerebellar cortex and, less so, in the thalamus and the bilateral brain stem and deep cerebellar nuclei. This hypometabolism was consistent with the unilateral and bilateral projections of the ablated cortex and with a decrease in transsynaptic activity. This deafferenta-tion remote from the lesion is a functional depression called diaschisis. At 8 weeks, before maximal recovery, the animals used the affected hindlimb for ambulation and made incomplete extension movements for reaching with the right forelimb. The investigators found partial recovery of metabolic activity in some of the ipsilateral thalamic nuclei, complete recovery in the contralateral thalamus, and up to moderate restoration in the other regions. The vestibular nuclei increased their activity at 1 and 8 weeks, perhaps as a compensatory mechanism that increased extensor postural reflexes. The investigators suggested that connections from other cortical areas that project to the caudate and putamen may have accounted for the increase in glucose utilization and improved function. Other mechanisms that might have contributed include enhanced activity of interneurons within the affected striatal neuronal groups, increased activity from subcortical projections, and sprouting of fibers from undamaged axons within the caudate and putamen or from projections from other sites.342
and fall one or more times over the weeks and months following injury.
Microarray and other gene identification technologies will help investigators study and manipulate these cascades.21 The chips for oligonucleotide and cDNA microarray analysis allow the investigator to identify the differences in tissues or cells in different states and monitor the expression of an enormous number of genes at any point in time.21 The microarray technique will allow investigators to discern similarities and differences between rodent models of injury and repair and the sequences of gene changes in primates. For example, in a rodent stroke model, ischemia conditioned neurons and glia to turn on from 30 to 40 genes that have reparative potential (see Experimental Case Study 2-2). A future step is to manipulate sustained expression of genes for neural repair and turn genes on and off as needed.
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