In this study we present further evidence supporting the reciprocal nature of output effects on forearm flexor and extensor muscles from single corticomotoneuronal (CM) cells. Spike-triggered averaging of rectified EMG activity was used to test the output effects of 105 motor cortex cells in two rhesus monkeys (Macaca mulatta) trained to perform alternating wrist movements and power grip. The electromyographic (EMG) activity was recorded from six forearm flexor and six forearm extensor muscles through pairs of percutaneously inserted intramuscular stainless steel wires. CM cells were identified by their characteristic postspike facilitation (PSF) in spike-triggered averages of agonist muscle EMG activity. Agonist muscles are those which coactivate with the cortical cell during movement. Of 105 motor cortex cells tested, 56 (53%) had no effect on either agonist or antagonist muscles. Of 49 cells that produced PSF of the agonist muscles, 14 (29%) also produced clear postspike suppression (PSS) of the antagonist muscles. Reproducibility of postspike effects was demonstrated by comparing spike-triggered averages of full-wave rectified EMG with averages of the same EMG activity triggered from randomly generated pulses. Consecutive averages from random triggers never showed consistent postspike effects. As a further test that our postspike effects were real, we computed averages of simulated EMG activity from the spikes of CM cells with reciprocal output effects. None of these averages showed consistent postspike effects. The mean onset latency of PSF calculated from 14 reciprocal CM cells yielding 51 PSF effects was 6.3 ms compared with 10.1 ms for 28 PSS effects from the same cells. PSS effects from a particular CM cell were nearly always longer in latency than the cell's PSF effects; only 2 of 28 PSS onset latencies were shorter than the longest latency PSF onset from the same cell. Average peak latencies for PSF and PSS were 8.6 and 11.6 ms, respectively. The magnitude of postspike effects was expressed as the percent of peak facilitation above the base-line mean for PSF or peak suppression below the base-line mean for PSS. With this measure, the average magnitude of PSF was 7.0% compared with 4.1% for reciprocal PSS. There was no correlation between onset latency and magnitude of PSF or PSS, although strong PSFs tended to have shorter latencies. Concerning the distribution of postspike effects, the average reciprocal CM cell facilitated 3.8 agonist muscles and suppressed 2.1 antagonist muscles. EDC was facilitated by all extension-related reciprocal CM cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Oxidative electrochemical pretreatment of carbon fibers greatly Improves their sensitivity for In vivo electrochemical detection of catecholamine species. It Is shown that the extent of the anodic potential excursion In the pretreatment Is a major factor In both the sensitivity and the response time of the resulting fiber electrode. The high sensitivity for neurotransmitter species such as dopamine appears mainly due to adsorption on the oxidized carbon fiber surface states. Practical protocols for fiber electrodes to be used In In vivo brain studies are evaluated.

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OBJECTIVE -The purpose of this study was to determine the effect of monochromatic infrared energy (MIRE) on plantar sensation in subjects with diabetic peripheral neuropathy.RESEARCH DESIGN AND METHODS -In this randomized, double-blind, placebocontrolled study, 39 subjects with diabetic peripheral neuropathy completed the 8-week study. Subjects received 30 min of active or placebo MIRE three times a week for 4 weeks. Plantar sensation was tested with monofilaments at the beginning of the study (M1), following 4 weeks of treatment (M2), and after an additional 4 weeks of nontreatment (M3). The number of sites that could sense the 5.07 monofilament was totaled at M1, M2, and M3. Data were analyzed using a special repeated-measures statistic followed by a post hoc Tukey-Kramer test.RESULTS -The average number of sites that patients could sense the 5.07 monofilament increased for both the active and placebo groups. There were significant gains from M1 to M2 (P Ͻ 0.002), no significant gains from M2 to M3 (P ϭ 0.234), and significant gains from M1 to M3 (P Ͻ 0.002) for both the active and placebo groups. There were no significant differences between active and placebo groups at any measurement.CONCLUSIONS -Thirty minutes of active MIRE applied 3 days per week for 4 weeks was no more effective than placebo MIRE in increasing sensation in subjects with diabetic peripheral neuropathy. Clinicians should be aware that MIRE may not be an effective modality for improving sensory impairments in patients with diabetic neuropathy. Diabetes Care 28:2896 -2900, 2005D iabetes is an increasingly prevalent disease that can have serious complications resulting in escalating health care costs. Recent reports indicate that over 18 million Americans have diabetes (1-3) and almost 30% of adults with diabetes have peripheral neuropathy (4), which increases their risk for developing foot ulcers and contributes to the incidence of lower-extremity amputations (3,5-10). The total cost attributed to managing patients with diabetes in the U.S. was an estimated $132 billion in 2002 (3).Screening for peripheral neuropathy in patients with diabetes is recommended to identify individuals at risk for foot ulcerations and lower-extremity amputations (11-16). After confirming peripheral neuropathy and the loss of protective sensation, treatment usually focuses on education in foot care and regular foot assessment (9,16). More recently, however, a variety of health care professionals have used devices that produce monochromatic infrared energy (MIRE) in an attempt to improve lower-extremity sensation in patients with peripheral neuropathy. MIRE devices were approved by the Food and Drug Administration in 1994 to increase circulation and reduce pain (17,18). There are reports in the literature of the use of MIRE for treating patients with wounds (19) and soft-tissue trauma (20), but several recent studies (21-26) describe the use of MIRE in treating patients with lower-extremity sensory neuropathy. In two separate uncontrolled studies (21,22), MIRE was...

Background: The origin of the dorsal scapular artery to the rhomboid muscles in humans has been the subject of uncertainty. The present study sought to clarify which of its two most common sources (the transverse cervical artery or the subclavian artery) is the major source of the dorsal scapular artery. Methods: Gross anatomical dissection was used to visualize the origin and course of the dorsal scapular artery in human cadavers.Results: We found that the dorsal scapular artery typically arises from either of two main sources: the subclavian artery (about 75% of all sides) or the transverse cervical artery (about 25% of all sides). Subclavian origins were approximately equally divided between its second and third part. Other origins for the dorsal scapular artery were negligible in frequency. Those dorsal scapular arteries that arose from the subclavian artery passed between the upper and middle or middle and lower trunks of the brachial plexus to course to the rhomboid muscles. In the case of transverse cervical artery origin, the dorsal scapular artery arose as a branch that passed deep to the levator scapulae muscle before coursing to the rhomboid muscles. No noteworthy differences were observed between males and females.Conclusions: These results strongly support the simple view, which does not appear widely accepted, that the subclavian artery is the most common source of the dorsal scapular artery to the rhomboid muscles and the transverse cervical artery a major but secondary source. o 1996 Wiley-Liss, Inc.