Background: Short- (SICI) and long-interval intracortical inhibition (LICI) are involved in the control of movement and movement initiation. Alterations to the two circuits can result in direct alterations to the physiology of the muscles and can be used to explain the physiological changes to individuals with spinal cord injury (SCI). Objective: To probe changes in GABAergic function by characterizing the recruitment curves of SICI and LICI interval intracortical inhibition in an upper limb muscle in chronic SCI participants with injury between C3 and C7. Methods: Recruitment curves were elicited with conditioning stimulus intensities determined as a percentage of active motor threshold (AMT) (SICI, 60% to 110% AMT; LICI, 90% to 130% AMT) and recorded from the flexor carpi radialis muscle during an isometric contraction equal to 15% to 20% of maximum voluntary contraction. Results: AMT was greater and motor-evoked potential sizes were lower in SCI compared with uninjured controls. SICI magnitude was not different between groups, although the range of conditioning stimulus intensities to evoke SICI was unique to each group. LICI was reduced in the control group during active contraction and remained present in SCI. Discussion: LICI was increased in the actively contracted flexor carpi radialis muscle in individuals with SCI compared with age-matched controls. These findings indicate that GABAB function mediating LICI is different in SCI versus controls. Conclusions: Increased LICI in SCI may be attributed to the medication baclofen or to changes in the neural mechanisms controlling contraction-related modulation of the LICI circuit.

Subjective and mild cognitive impairment (SCI and MCI) are etiologically heterogeneous conditions. This poses problems for assessment of pathophysiological mechanisms and risk of conversion to dementia. Neuropsychological, imaging, and cerebrospinal fluid (CSF) findings serve to distinguish Alzheimer’s disease (AD) and other etiological subgroups. Tau-molecules stabilize axonal microtubuli; high CSF total tau (T-tau) reflects ongoing axonal damage consistent with AD. Here, we stratify patients by CSF T-tau pathology to determine if memory network diffusion tensor imaging (DTI) predicts memory performance in the absence of elevated T-tau. We analyzed neuropsychological test results, hippocampus volume (HcV) and white matter diffusivity in 45 patients (35 with normal T-tau). The T-tau pathology group showed more hippocampus atrophy and memory impairment than the normal T-tau group. In the T-tau normal group: (1) memory was related with white matter diffusivity [fractional anisotropy (FA) and radial diffusivity (DR)], and (2) FA of the genu corpus callosum was a unique predictor of variance for verbal learning, and HcV did not contribute to this prediction. The smaller sample size in the T-tau pathology group precludes firm conclusions. In the normal T-tau group, white matter tract and memory changes may be associated with normal aging, or with non-tau related pathological mechanisms. (JINS, 2010, 16, 58–69.)