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Biomedical subjects

K C Hayes

Publications and source records attributed to K C Hayes.

At least 91 records · Page 5Linked to original sources
PubMed1992

Afferent conditioning of motor evoked potentials following transcranial magnetic stimulation of motor cortex in normal subjects.

The present study determined the effects of percutaneous electrical stimulation of the plantar surface on motor evoked potentials (MEPs) in tibialis anterior (TA) and soleus (SOL) of normal subjects following transcranial magnetic stimulation of motor cortex. The conditioning stimulation consisted of a 20 msec train of electrical pulses (500 Hz; 0.1 msec rectangular) delivered to the medial border of the sole of the foot at an intensity just subthreshold for evoking a flexion reflex. The conditioning (C) stimulation preceded the test (T) cortical stimulation by intervals of 20-130 msec. Magnetic stimulation of motor cortex (Cadwell MES-10) was delivered through a 9.5 cm focal point coil positioned tangential to the scalp and located with the rim over vertex. Five healthy adults served as subjects and each was investigated on at least 2 occasions. At C-T intervals 20-50 msec there was a mild inhibition of MEPs in both TA and SOL. This was followed by marked facilitation (greater than 300%) of MEPs at C-T intervals 50-85 msec in both TA and SOL in all subjects. At longer C-T intervals greater than 110 msec, there was an inhibition of MEPs in TA but not in SOL. Based on the time course of these 3 phases of MEP amplitude modulation, and different stimulation thresholds for each phase, it appears that separate neurophysiological processes underlie each phase of MEP modulation. These observations also suggest that percutaneous electrical stimulation may be useful as a means of enhancing low amplitude or subliminal MEPs in normal subjects or patients with myelopathy.

Adaptation, Physiological↗
PubMed1992

Reinforcement of subliminal flexion reflexes by transcranial magnetic stimulation of motor cortex in subjects with spinal cord injury.

A 20 msec train (500 Hz; 0.1-0.2 msec duration) of percutaneous electrical stimulation (ES) applied to the plantar surface was used to condition muscle responses evoked in tibialis anterior (TA) by transcranial magnetic stimulation of the motor cortex in 8 subjects with traumatic spinal cord injury (SCI). The intensity of conditioning ES was adjusted to just subthreshold for evoking flexion reflexes in TA and was delivered at conditioning-test (C-T) intervals of 15-60 msec prior to cortical stimulation. Four subjects with clinically complete SCI revealed no muscle response to cortical stimulation or following combined subliminal percutaneous ES and cortical stimulation. Four subjects (3 clinically incomplete and 1 complete injury) demonstrated muscle responses with a latency of 70-80 msec time-locked to the percutaneous ES when the conditioning subliminal stimulation was delivered at C-T: 15-40 msec. These responses, resembling suprathreshold flexion reflexes, reflect the convergence of excitatory afferent and cortical inputs and provide evidence of preserved corticospinal innervation to the L4-5 segmental motoneuron or interneuron pools. In 3 of the subjects this preserved corticospinal influence was evident despite absence of motor evoked potentials (MEPs) following cortical stimulation. The effect of the combined electrical and cortical stimulation in yielding suprathreshold flexion reflexes, instead of the facilitated MEPs seen in control subjects, appears to be related to slowed central conduction, prolonged temporal dispersion of the motoneuron facilitation following cortical stimulation and segmental reflex changes associated with disrupted modulation of interneuronal pathways. The results show this conditioning paradigm to be useful in revealing preserved corticospinal innervation in some SCI subjects with absent MEPs.

Adaptation, Physiological↗
PubMed1992

Modulation of infant formula fat profile alters the low-density lipoprotein/high-density lipoprotein ratio and plasma fatty acid distribution relative to those with breast-feeding.

The effect of breast-feeding was compared with that of two fat-modified milk formulas in 45 infants (15 per group) studied by assessing body weight gain for 4 months and plasma lipids, lipoprotein profiles, fatty acid profiles of plasma and red blood cells, and plasma tocopherol status 3 months after birth. A saturated fat formula with coconut oil/soybean oil (COCO/SOY) had a fatty acid content and polyunsaturated/saturated ratio (P/S, 0.55) comparable with that of human milk fat (P/S, 0.39) and had the same fat energy content (50% kcal). The second formula, with corn oil/soybean oil (CORN/SOY), was highly unsaturated (P/S, 4.6), with only 35% kcal from fat. Energy intake and body weight gain were similar for all groups. Plasma total cholesterol, triglyceride, and phospholipid levels were significantly lower (greater than 20% on average) in infants fed the CORN/SOY formula than in infants fed either the COCO/SOY formula or human milk. Infants fed the CORN/SOY formula also had lower (25% to 35%) plasma low-density lipoprotein cholesterol and apolipoprotein B levels and low-density lipoprotein/high-density lipoprotein and apolipoprotein B/apolipoprotein A-I ratios. Plasma, red blood cell, and cholesteryl ester fatty acids from infants fed COCO/SOY contained less 18:1 and more 18:2; cholesterol esters in plasma from breast-fed infants had the highest 20:4n-6 levels. Plasma tocopherol levels were higher in infants consuming formulas. The presence of cholesterol in human milk appeared to expand the low-density lipoprotein pool and exert an "unfavorable" increase in the low-density lipoprotein/high-density lipoprotein ratio. Thus modulation of infant lipoproteins by changing dietary fat and cholesterol is feasible and in keeping with the known response in adults.

Apolipoproteins↗
PubMed1992

Bacterial biofilm formation in the urinary bladder of spinal cord injured patients.

Ten spinal cord injured patients aged 8 to 55 years (mean 32) were followed for up to 2 months after admission to a rehabilitation setting from an acute care hospital. Urinary fluid and bladder epithelial cells were collected weekly by intermittent catheterization and examined for bacterial colonization. Six patients had no history of urinary tract infection upon admission, likely due to the antimicrobial coverage given during acute care. All the patients subsequently became colonized with uropathogens at some time during the study period. Bacterial biofilms were found in 73% of the samples (73% Gram negative organisms, 27% Gram positive), with mean pathogenic adhesion counts of 29 organisms per bladder cell. In 16% of cases, bladder biofilms were found when urine culture was negative. Bacterial biofilms were also evident during antimicrobial therapy in 10 of 12 samples tested and urine cultures showed breakthrough infections in 50% of cases. Two asymptomatic patients were colonized with Klebsiella pneumoniae and Pseudomonas aeruginosa and were dismissed without requiring therapy. Clearly, bacterial biofilms can exist on bladder epithelia, without being detected in urine samples and without giving rise to symptoms. The extent to which they occur and damage the host remains to be determined, as does the answer to the question, should these patients be treated?

Adult↗
PubMed1992

Reliability of labial closure force measurements in normal subjects and patients with CNS disorders.

This study determined the reliability of maximal upper and lower lip closing forces measured using a strain-gauged cantilever beam assembly. An intraclass correlation approach was used to explicitly partition the "error free" between-subject variance and measurement error variance across repeated days (2) and across repeated trials (5). Ten healthy adults served as controls and 30 patients with diagnoses of multiple sclerosis, cerebrovascular accident, or Parkinson's disease served as subjects. The intraclass correlation analyses revealed generally high reliability (R greater than .90) for upper and lower lip force measurements, for various combinations of control and/or patient groups, and within each individual patient group. There was moderate correspondence between the quantitative measures of lip force and the clinical assessment of combined upper (r = .67) and lower lip closure force (r = .62) but low correspondence between the quantitative measures of lip force and the presence of motor speech deficit. The lower lip force of patients with Parkinson's disease (M = 3.1 N) on Day 1 was markedly reduced from that of all other patient groups and controls (M = 10.1 N). These results yield helpful information for the design of investigations of oral-motor weakness and for the quantitative assessment of an individual's clinical status.

Aged↗
PubMed1992

Vegetarians have higher plasma alpha-tocopherol relative to cholesterol than do nonvegetarians.

Biological antioxidants are thought to play a protective role in certain disease processes, including atherosclerosis. To compare the relative antioxidant/atherogenic risk between vegetarians (presumed lower risk) and omnivores (higher risk), the alpha-tocopherol, total cholesterol and fatty acid (FA) profiles were determined in the plasma of 79 vegetarians (28 males, 51 females) and 79 age- and sex-matched nonvegetarians. In the vegetarian group, mean (+/- SEM) plasma alpha-tocopherol was 714 +/- 46 micrograms/dl for males and 725 +/- 24 for females; corresponding cholesterol values were 122 +/- 5 mg/dl and 138 +/- 3, respectively, which were significantly lower than the respective control values (928 +/- 38; 883 +/- 23 and 206 +/- 6; 188 +/- 4). However, when plasma tocopherol was expressed in terms of cholesterol, the tocopherol: cholesterol molar ratio was significantly enhanced for both male (27%) and female (11%) vegetarians. Vegetarians also had a lower atherosclerosis risk based on their plasma FA profile (higher linoleic:oleic acid ratio) which correlated well (r = 0.72; p less than 0.001) with plasma alpha-tocopherol:cholesterol molar ratio. Since the bulk of tocopherol is transported in low-density lipoprotein, this lipoprotein in vegetarians may be better protected against lipid peroxidation, a process believed to be important in the pathogenesis of atherosclerosis.

Adult↗
PubMed1992

Dietary palmitic and oleic acids exert similar effects on serum cholesterol and lipoprotein profiles in normocholesterolemic men and women.

To compare the effects of dietary palmitic acid (16:0) vs oleic acid (18:1) on serum lipids, lipoproteins, and plasma eicosanoids, 33 normocholesterolemic subjects (20 males, 13 females; ages 22-41 years) were challenged with a coconut oil-rich diet for 4 weeks. Subsequently they were assigned to either a palm olein-rich or olive oil-rich diet followed by a dietary crossover during two consecutive 6-week periods. Each test oil served as the sole cooking oil and contributed 23% of dietary energy or two-thirds of the total daily fat intake. Dietary myristic acid (14:0) and lauric acid (12:0) from coconut oil significantly raised all the serum lipid and lipoprotein parameters measured. Subsequent one-to-one exchange of 7% energy between 16:0 (palm olein diet) and 18:1 (olive oil diet) resulted in identical serum total cholesterol (192, 193 mg/dl), low-density lipoprotein cholesterol (LDL-C) (130, 131 mg/dl), high-density lipoprotein cholesterol (HDL-C) (41, 42 mg/dl), and triglyceride (TG) (108, 106 mg/dl) concentrations. Effects attributed to gender included higher HDL in females and higher TG in males associated with the tendency for higher LDL and LDL/HDL ratios in men. However, both sexes were equally responsive to changes in dietary fat saturation. The results indicate that in healthy, normocholesterolemic humans, dietary 16:0 can be exchanged for 18:1 within the range of these fatty acids normally present in typical diets without affecting the serum lipoprotein cholesterol concentration or distribution. In addition, replacement of 12:0 + 14:0 by 16:0 + 18:1, but especially 16:0 or some component of palm olein, appeared to have a beneficial impact on an important index of thrombogenesis, i.e., the thromboxane/prostacyclin ratio in plasma.

Adult↗
PubMed1992

Comparison between the effects of dietary saturated (16:0), monounsaturated (18:1), and polyunsaturated (18:2) fatty acids on plasma lipoprotein metabolism in cebus and rhesus monkeys fed cholesterol-free diets.

Cebus and rhesus monkeys were fed cholesterol-free diets providing 40% of energy as fat for 6-wk periods. The fats were high-linoleic acid safflower oil (HLSO), high-oleic acid safflower oil (HOSO), or palm oil (PO), rich in polyunsaturated (18:2), monounsaturated (18:1), or saturated (16:0) fatty acids, respectively. In cebus monkeys, plasma cholesterol concentrations during HLSO intake were 17-19% lower than those during HOSO or PO intake, attributed to a decrease in high-density lipoprotein (HDL). Plasma triglyceride (TG) and low-density-lipoprotein (LDL) cholesterol concentrations were comparable during all dietary treatments. Sixty-eight percent of total LDL catabolism was receptor mediated in all dietary groups and this was associated with similar apolipoprotein B pool sizes and fractional catabolic rates. Rhesus monkeys revealed similar cholesterol concentrations (total, LDL, and HDL) during all dietary treatments. TG concentrations during PO intake were 34% and 63% higher than those during HOSO and HLSO intakes, respectively. Hence, dietary 16:0 and 18:1 produce similar effects on LDL and HDL metabolism in normocholesterolemic primates.

Animals↗
PubMed1992

Dietary fat and cholesterol modulate the plasma lipoprotein distribution and production of pigment or cholesterol gallstones in hamsters.

To evaluate the impact of key dietary factors on plasma lipoproteins and gallstone induction, male Syrian hamsters were fed either cholesterol and fat-supplemented purified diets containing glucose or lactose, or cholesterol and fat-free diets with or without fiber, for 13 wk. Fat-supplemented hamsters were hyperlipidemic in comparison to those fed fat-free diets. The former group revealed a greatly expanded VLDL fraction, whereas a normal HDL2 pool predominated in the latter group. Plasma fatty acids indicated that hamsters fed the fat-free diet were essential fatty acid deficient whilst the hamsters fed the fat-supplemented diet were subnormal in essential fatty acids. Ninety-three percent of the hamsters fed the fat-supplemented diet had gallstones (mostly cholesterol), whereas 62% of hamsters fed the fat-free diet had gallstones (almost all pigmented). Lactose increased cecal weight and prevented pigment stone formation in the fat-supplemented hamsters, whereas adding fiber to the fat-free diet contributed essential fatty acids, eliminated cholesterol stones and enhanced pigment stone formation. Thus, diets containing casein, rice flour, glucose and fiber with minimal essential fatty acids but no cholesterol promoted pigment stones (associated with a normal lipoprotein profile); a low fat diet limited in essential fatty acids but containing cholesterol and lactose, promoted cholesterol gallstones (associated with an expanded VLDL pool).

Adipose Tissue↗
PubMed1992

Dietary fatty acid thresholds and cholesterolemia.

Results obtained with cebus monkeys indicate that dietary myristic (14:0) and palmitic (16:0) acids exert disparate effects on cholesterol metabolism, whereas the ability of linoleic acid (18:2) to decrease total plasma cholesterol displays an upper limit or threshold. Reanalysis of published data suggests a similar situation pertains in humans. In agreement with an earlier human study, 14:0 appears to be the principal saturated fatty acid that raises plasma cholesterol whereas 18:2 lowers it. Oleic acid (18:1) appears neutral. The effect of 16:0 may vary. In normocholesterolemic subjects consuming diets containing less than or equal to 300 mg/day of cholesterol, 16:0 appears to be without effect on plasma cholesterol. However, in hypercholesterolemic subjects (greater than 225 mg/dl) and especially those consuming diets providing cholesterol intakes of greater than or equal to 400 mg/day, dietary 16:0 may expand the plasma cholesterol pool.

Animals↗
PubMed1992

Dietary impact on biliary lipids and gallstones.

Although dietary factors influence bile lithogenicity and gallstone formation, the main dietary effect appears to be indirect, depending on an interaction between caloric consumption and gender-specific aspects of lipoprotein metabolism. Excessive energy intake elicits its detrimental effect by altering lipoprotein and hepatic cholesterol metabolism in association with hyperinsulinemia. Factors, dietary and genetic, that favor elevated hepatic cholesterol synthesis and production of a bile acid profile in which chenodeoxycholic acid predominates appear to be associated with lithogenic bile. An inconsistent effect of dietary fat saturation on gallstones is that polyunsaturates possibly increase risk in men and decrease risk in women. Vegetable protein may reduce the risk of cholelithiasis. Whereas both the amount and type of dietary fiber influence cholesterol and bile lipid metabolism, specific associations between fiber and gallstones in humans remain elusive.

Animals↗
PubMed1992

Low density lipoprotein from humans supplemented with n-3 fatty acids depresses both LDL receptor activity and LDLr mRNA abundance in HepG2 cells.

Fish oil supplementation in humans is often associated with an expanded low density lipoprotein (LDL) pool that is not thought to reflect increased production. Since data on clearance of LDL after fish oil supplementation (FO-LDL) are equivocal, normal volunteers (four men and three women) received ten capsules containing 3.6 g eicosapentaenoic acid and 2.9 g docosahexaenoic acid (approximately 2.5% total calories as methyl esters) for 2 weeks. Total plasma cholesterol was unchanged, but triglycerides decreased 30%. Low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were unchanged. Analysis of the LDL particles revealed that increased esterified cholesterol caused the FO-LDL core/surface ratio to be greater than baseline LDL (BL-LDL), resulting in a shift in mean LDL density from 1.060 to 1.056. N-3 fatty acids in FO-LDL were also increased greater than 40% at the expense of n-6 and n-9 fatty acids. Human hepatoma HepG2 cells were used to study the effects of FO-LDL on LDL receptor activity and mRNA abundance for the LDL receptor, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, and various apolipoproteins associated with cholesterol metabolism. In this system FO-LDL reduced LDL receptor activity compared to BL-LDL. Scatchard analysis revealed that LDL receptor number (Bmax) was reduced to one-third normal (P less than 0.001) whereas particle binding affinity was unchanged. The mRNA abundance for the LDL receptor and apoA-I were also depressed, even by low concentrations (10 micrograms/ml and 20 micrograms/ml LDL protein) of FO-LDL as compared to BL-LDL. HepG2 cells incubated with FO-LDL had decreased cellular free cholesterol but increased cholesteryl esters. Thus, moderate supplementation with fish oil n-3 fatty acids in normal humans enriches their LDL particles in cholesteryl esters and n-3 fatty acids. These particles depress both LDL receptor activity and LDL receptor mRNA abundance in HepG2 cells.

Apolipoproteins↗
PubMed1991

Dietary fat saturation in rhesus monkeys affects LDL concentrations by modulating the independent production of LDL apolipoprotein B.

In a recent study from this laboratory, rhesus monkeys fed a 90% palm oil/10% soybean oil-containing diet (PS), rich in 16:0 and 18:1 fatty acids, had decreased total and LDL cholesterol concentrations compared to monkeys fed a 90% coconut oil/10% soybean oil-containing diet (CS), rich in 12:0 and 14:0 fatty acids. To investigate the metabolic basis of these changes, homologous 125I-VLDL and 131I-LDL were injected simultaneously into eight monkeys (four per dietary group). Analysis of apo B specific activity curves revealed that PS monkeys had an increased pool size of VLDL apo B (P less than 0.02), a 3-fold increase in the total VLDL apo B transport rate (P less than 0.001), a decreased pool size of LDL apo B (P less than 0.01) and a 2-fold decrease in the total transport rate of LDL apo B (P less than 0.001), while the irreversible FCR for VLDL apo B and LDL apo B was similar between dietary groups. PS monkeys derived a greater percentage of LDL apo B from VLDL catabolism resulting in a greater transport rate of LDL apo B from VLDL catabolism (P less than 0.055), in comparison to CS monkeys. For CS monkeys the proportion as well as the amount of LDL apo B derived from VLDL-independent catabolism (i.e., LDL apo B derived from sources other than VLDL catabolism) was higher (P less than 0.001) than the values obtained in PS monkeys. In both dietary groups the proportion of VLDL apo B converted to LDL apo B was similar, although the absolute amount was higher for the PS monkeys (P less than 0.06). The proportion of VLDL apo B directly removed from the circulation was similar for both dietary groups, with the absolute amount being higher for the PS monkeys (P less than 0.001). Consistent with the lower pool size of LDL apo B and the higher pool size of VLDL apo B observed in PS monkeys, plasma and LDL cholesterol concentrations tended to be lower, whereas plasma triacylglycerol and VLDL cholesterol concentrations tended to be higher, but these changes were not statistically significant. Although total apo B and VLDL apo B transport rates were increased 2-3-fold in PS monkeys, LDL apo B concentration was reduced by 40% (P less than 0.02) attributed to a significant reduction in the mass and proportion of LDL apo B derived independent of VLDL catabolism.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Diet-induced type IV-like hyperlipidemia and increased body weight are associated with cholesterol gallstones in hamsters.

Male Syrian hamsters (60-70 g) were fed purified diets containing 5% fat (American Fat Blend) and 15% fiber with or without 0.3% cholesterol (0.86 mg/kcal), for 12 weeks. Hamsters fed the cholesterol-supplemented challenge diet revealed a major increase in plasma triglyceride between 9 and 12 weeks, whereas plasma cholesterol (which reflected body weight dynamics) increased three-fold up to nine weeks and plateaued (342 +/- 22 vs. 122 +/- 5 mg/dL). The greatest increases in cholesterol occurred in the very low density lipoprotein (VLDL) and high density lipoprotein (HDL2) fractions. Gallstone incidence was similar (69% vs. 78%) for cholesterol-supplemented vs. control hamsters, but the type of stones differed. Of the cholesterol-supplemented hamsters with gallstones, 45% had cholesterol stones and 55% had pigment stones. Only pigment stones were seen in control hamsters. Hamsters with cholesterol stones were 25% heavier and transported most cholesterol in VLDL (33 +/- 5%), approximately double that in VLDL of cholesterol-supplemented hamsters with no stones (19 +/- 3%) or cholesterol-supplemented hamsters with pigment stones (21 +/- 3%). Hamsters with pigment stones or no stones (regardless of diet fed) transported the majority of their cholesterol in HDL2 (44%), whereas this figure was only 27% in hamsters that developed cholesterol stones. Thus pigment stones develop routinely in hamsters fed casein-based purified diets. Adding dietary cholesterol resulted in cholesterol gallstones only in those hamsters that gained the most weight and whose terminal VLDL/HDL cholesterol ratio exceeded 1.0, not unlike the lipoprotein profile of obese humans who develop cholesterol gallstones.

Animals↗
PubMed1991

Species variation in the atherogenic profile of monkeys: relationship between dietary fats, lipoproteins, and platelet aggregation.

Because lipoproteins and platelet aggregation have been implicated in atherogenesis, relative differences in the response of these variables to dietary fat saturation were compared in three species of monkeys differing in their susceptibility to atherosclerosis (cebus, rhesus, and squirrel monkeys). Both long-term (8-12 years) and short-term (8 weeks) responses to diets containing 31% fat calories were examined in the same monkeys. As expected, long-term feeding of coconut oil by comparison to corn oil produced significantly higher plasma concentrations of total cholesterol, LDL cholesterol, apoB, and triglycerides, as well as higher ratios of LDL/HDL cholesterol and apo B/apo A-I. These responses were characteristic of all species with cebus being most responsive and rhesus the least. The short-term plasma cholesterol response to animal fats (butter, lard, beef tallow) was significantly less than that to coconut oil. When fish oil was substituted for two-thirds of either corn oil or coconut oil, exceptional decreases occurred in plasma cholesterol and triglycerides, as well as in HDL cholesterol and apo A-I concentrations despite the fact that the fish oil diets contained more saturated fat and less polyenes than the corn oil diet. Platelet aggregation tended to increase with saturated fat consumption and greatly decreased with fish oil intake in all monkeys, although cebus monkeys were ten-fold more resistant to platelet aggregation than the other two species. The molecular species of platelet phosphatidylcholine (PC) varied with both the dietary fat fed and species of monkey. An inverse correlation (r = -0.60; p less than 0.001) was found between changes in one such PC molecular species (18:0-20:4) induced by diet and the platelet aggregation threshold. These results demonstrate that the lipemic and platelet responses to dietary saturated fat depend upon both the type of fat (i.e., the specific combination of dietary fatty acids, including the chain length of saturated fatty acids and the degree of polyunsaturation) and the species of monkey (genetic component) in which the response is elicited.

Animals↗
PubMed1991

Dietary saturated fatty acids (12:0, 14:0, 16:0) differ in their impact on plasma cholesterol and lipoproteins in nonhuman primates.

Three species of monkey (rhesus, cebus, and squirrel) were rotated through five purified diets containing 31% energy as various fat blends (P:S between 0.1 and 1.0) for 12-wk periods to compare the impact of specific dietary fatty acids on plasma lipids and lipoproteins. As 12:0 + 14:0 was replaced by 16:0, a significant decrease occurred in total and LDL cholesterol, whereas slight increases in total cholesterol and the LDL-HDL ratio occurred when 16:0 replaced 18:2. Hegsted and Keys regression equations provided a good fit for the observed data, but the predicted total cholesterol response was perfect (r = 0.995) for both equations when 16:0 was considered neutral. Thus, under these conditions 16:0 was less cholesterolemic than 12:0 + 14:0 and only slightly cholesterolemic compared with 18:2.

Animals↗
PubMed1991

Intramuscular recording of H-reflexes from muscles of the posterior compartment of the lower leg.

This study was designed to elucidate the role of different muscles of the posterior compartment of the lower leg in the generation of the surface-recorded H-reflex. H-reflexes were evoked through percutaneous stimulation of the posterior tibial nerve and recorded concurrently, using monopolar electrodes from the soleus (SOL), medial and lateral gastrocnemii (MG and LG), tibialis posterior (TP), flexor digitorum longus (FDL), and flexor hallucis longus (FHL). There were significant (P less than 0.01) differences in the amplitudes, latencies, and modified H:M ratios of the responses recorded from the different muscles. The SOL modified H:M ratios were consistently the highest (x = 1.02), while the H:M ratios for MG (x = 0.34) and LG (x = 0.37) were consistently the lowest. Latencies of H-reflexes obtained from proximal recording sites (x = 29.2 ms) were significantly shorter than those from the most distal site (x = 31.5 ms). These results establish the contribution made by various deep and superficial muscles to the conventionally recorded H-reflex and help explain the differences in H-reflex amplitudes and latencies when recordings are made from different sites.

Adult↗