Motor-evoked potentials (MEP) in the tibialis anterior (TA) muscle were shown to be facilitated by repetitive electrical stimulation of the common peroneal (CP) nerve at intensities above motor threshold. The TA electromyogram (EMG) and ankle flexion force were recorded in response to transcranial magnetic stimulation (TMS) of the leg area of the motor cortex to evaluate the excitability of cortico-spinal-muscular pathways. Repetitive stimulation of the CP nerve at 25 Hz for 30 min increased the MEP by 50.3 +/- 13.6% (mean +/- S.E.) at a TMS intensity that initially gave a half-maximum MEP (MEPh). In contrast the maximum MEP (MEPmax) did not change. Ankle flexion force (103 +/- 21.9%) and silent period duration (75.3 +/- 12.9%) also increased. These results suggest an increase in corticospinal excitability, rather than total connectivity due to repetitive CP stimulation. Facilitation was evident after as little as 10 min of stimulation and persisted without significant decrement for at least 30 min after stimulation. The long duration of silent period following CP stimulation (99.2 +/- 14.8 ms) suggests that this form of stimulation may have effects on the motor cortex. To exclude the possibility that MEPh facilitation was primarily due to sensory fibre activation, we performed several control experiments. Preferentially activating Ia muscle afferents by vibration in the absence of motor activity had no significant effect. Cutaneous afferent activation via stimulation of the superficial peroneal nerve increased the amplitude of responses at MEPmax rather than MEPh. Concurrent tendon vibration and superficial peroneal nerve stimulation failed to facilitate TA MEP responses. In summary, repetitive electrical stimulation of the CP nerve elicits lasting changes in corticospinal excitability, possibly as a result of co-activating motor and sensory fibres.

Following spinal cord injury (SCI), prolonged muscle spasms are readily triggered by brief sensory stimuli. Animal and indirect human studies have shown that a substantial portion of the depolarization of motoneurons during a muscle spasm comes from the activation of persistent inward currents (PICs). The brief (single pulse) sensory stimuli that trigger the PICs and muscle spasms in chronically spinalized animals evoke excitatory post-synaptic potentials (EPSPs) that are broadened to more than 500 ms, the duration of depolarization required to activate a PIC in the motoneuron. Thus, in humans, we investigated if post-synaptic potentials (PSPs) evoked from brief (<20 ms) sensory stimulation are changed after SCI and if they are broadened to > or =500 ms to more readily activate motoneuron PICs and muscle spasms. To estimate both the shape and duration of PSPs in human subjects we used peristimulus frequencygrams (PSFs), which are plots of the instantaneous firing frequency of tonically active single motor units that are time-locked to the occurrence of the sensory stimulus. PSFs in response to cutaneomuscular stimulation of the medial arch or toe of the foot, a sensory stimulus that readily triggers muscle spasms, were compared between non-injured control subjects and in spastic subjects with chronic (>1 year), incomplete SCI. In non-injured controls, a single shock or brief (<20 ms) train of cutaneomuscular stimulation produced PSFs consisting of a 300 ms increase in firing rate above baseline with an interposed period of reduced firing. Parallel intracellular experiments in motoneurons of adult rats revealed that a 300 ms EPSP with a fast intervening inhibitory PSP (IPSP) reproduced the PSF recorded in non-injured subjects. In contrast, the same brief sensory stimulation in subjects with chronic SCI produced PSFs of comparatively long duration (1200 ms) with no evidence for IPSP activation, as reflected by a lack of reduced firing rates after the onset of the PSF. Thus, unlike non-injured controls, the motoneurons of subjects with chronic SCI are activated by very long periods of pure depolarization from brief sensory activation. It is likely that these second-long EPSPs securely recruit slowly activating PICs in motoneurons that are known to mediate, in large part, the many seconds-long activation of motoneurons during involuntary muscle spasms.

This article describes a single case of migraine headaches misdiagnosed as idiopathic intracranial hypertension in a young woman. The implications of such a diagnosis are discussed. Literature regarding normal intracranial pressure is reviewed.

Background and Purpose-Diffusion-weighted MRI (DWI) demonstrates ischemic tissue with high sensitivity. Although low cerebral blood volume (CBV) is also used as a marker for infarction, the quantitative relationship between diffusion abnormalities and CBV is unknown. We tested the hypothesis that CBV would decrease proportionally to the apparent diffusion coefficient in patients with acute stroke and thus could be used as a surrogate parameter for diffusion restriction. Methods-Perfusion-weighted imaging and DWI was performed in 54 patients within 28 hours of symptom onset. Mean apparent diffusion coefficient, cerebral blood flow, and CBV were measured within DWI lesions and contralateral regions. Results-Within DWI lesions, CBV (3.3Ϯ1.9 mL/100 g) was significantly decreased relative to contralateral regions (4.1Ϯ2.1 mL/100 g, PϽ0.001). Relative CBV was not decreased in patients with evidence of early reperfusion (1.2Ϯ0.5) or mild stroke (National Institutes of Health Stroke Scale Ͻ4, 1.1Ϯ0.6). Linear regression indicated that relative CBV was predictive of relative apparent diffusion coefficient only in patients imaged within 9 hours of symptom onset (Rϭ0.50, Pϭ0.02). Ischemic tissue volumes generated using a CBV threshold of the 50th percentile of normal tissue were correlated with DWI lesion volumes (Rϭ0.73, PϽ0.001). The mean difference between the CBV threshold of the 50th percentile of normal tissue and DWI lesion volumes was 6.3 mL (95% limits of agreement, 0.1 to 12.6 mL). Conclusions-Decreases in relative CBV are predictive of diffusion abnormalities in ischemic stroke. The pattern of CBV changes varies with clinical severity and symptom duration. Ischemic tissue volumes comparable to DWI lesions can be generated using CBV thresholds, but the use of this method is limited in patients with minor stroke. (Stroke. 2010; 41:2795-2800.)