Background: Previous studies comparing paretic limb blood flow with the unaffected limb have been contradictory and have often omitted comparisons of peak reactive hyperemic flow. Our objective was to perform bilateral measurements of resting and reactive hyperemic blood flow in the lower legs of chronic (>6 months) stroke patients. A secondary purpose was to determine the extent to which any unilateral changes in limb blood flow were a function of decreases in lean tissue mass on the affected side. We hypothesized that the chronic hemiparesis accompanying ischemic stroke creates an altered metabolic environment in the tissues of the affected side that ultimately impairs vasomotor function. Methods: The study used a single-visit cross-sectional design. All tests were performed at the Baltimore VA Medical Center. Nineteen chronic hemiparetic stroke patients (15 male, 4 female) who had mild to moderate hemiparetic gait after ischemic stroke were recruited for observation. Bilateral measurements of resting and reactive hyperemic blood flow were made using venous occlusion strain gauge plethysmography. Paired t-tests were used for the between leg comparison. Regression analysis and analysis of covariance were utilized to determine the strength of the relationship between lower leg lean tissue mass and blood flow. Results: Resting and reactive hyperemic blood flows were significantly reduced in the paretic compared with the non-paretic limb (32 and 35%, respectively, p < 0.001). Lean tissue mass was also significantly lower in the affected limb (p < 0.01). However, neither resting nor reactive hyperemic blood flows were significantly correlated with lower leg lean tissue mass by dual energy X-ray absorptiometry. The difference in blood flow between limbs remained after covarying for lean tissue mass. Conclusion: Hemiparesis causes impairments in vasomotor function under both resting and hyperemic conditions that are independent of the muscle atrophy on the affected side.

1.
Williams GR, Jiang JG, Matchar DB, Samsa GP: Incidence and occurrence of total (first ever and recurrent) stroke. Stroke 1999;30:2523–2528.
2.
Gresham GE, Fitzpatrick TE, Wolf PA, McNamara PM, Kannel WB, Dawber TR: Residual disability in survivors of stroke – The Framingham Study. N Engl J Med 1975;293:954–956.
3.
Jorgensen HS, Nakayama H, Raaschou HO, Olsen TS: Recovery of walking function in stroke patients: The Copenhagen stroke study. Arch Phys Med Rehabil 1995;76:27–32.
4.
Ryan AS, Dobrovolny C, Silver KH, Smith GV, Macko RF: Hemiparetic muscle atrophy after stroke and increased intra-muscular fat. Arch Phys Med Rehabil 2002;83:1703–1707.
5.
Landin S, Hagenfeldt L, Saltin B, Wahren J: Muscle metabolism during exercise in hemiparetic patients. Clin Sci Mol Med 1977;53:257–269.
6.
Sarelius IH, Cohen KD, Murrant CL: Role of capillaries in coupling blood flow with metabolism. Clin Exp Pharmacol Physiol 2000;27:826–829.
7.
Berg BR, Cohen KD, Sarelius IH: Direct coupling between blood flow and metabolism at the capillary level in striated muscle. Am J Physiol 1997;272:H2693–H2700.
8.
Reis DJ, Wooten GF, Hollenberg M: Differences in nutrient blood flow of red and white skeletal muscle in the cat. Am J Physiol 1967;213:592–596.
9.
Ellis LB, Weiss S: Vasomotor disturbance and edema associated with cerebral hemiplegia. Arch Neurol Psychiatry 1936;36:362–372.
10.
Kennard MA: Vasomotor disturbances resulting from cortical lesions. Arch Neurol Psychiatry 1935;33:537–545.
11.
LaBan MM, Johnson EW: Velocity of blood flow in the saphenous vein of hemiplegic patients. Arch Phys Med Rehabil 1965;46:245–249.
12.
Goldberg MJ, Skowlund HV, Katke FJ: Comparison of circulation in the lower extremities of hemiplegic patients. Arch Phys Med Rehabil 1968;49:467–470.
13.
Duff F, Shepherd JT: The circulation in the chronically denervated forearm. Clin Sci 1953;12:407–416.
14.
Kozak P: Circulatory changes of the paretic extremities after acute anterior poliomyelitis. Arch Phys Med Rehabil 1968;49:77–81.
15.
Redisch W, Tangco FT, Werthheimer L, Lewis AJ, Steele JM: Vasomotor responses in the extremities of subjects with various neurologic lesions. Circulation 1957;15:518–524.
16.
Wanklyn P, Ilsley DW, Greenstein D, et al: The cold hemiplegic arm. Stroke 1994;25:1765–1770.
17.
Adams WC, Imms FJ: Resting blood flow in the paretic and nonparetic lower legs of hemiplegic persons: Relation to local skin temperature. Arch Phys Med Rehabil 1983;64:423–428.
18.
Hoerner EF, Dacso MM, McKeown J, Case H: Altered vasomotor changes (peripheral) in hemiplegias. Angiology 1954;5:414–428.
19.
Uprus V, Gaylor JB, Williams DJ, Carmichael EA: Vasodilation and vasoconstriction in response to warming and cooling the body: Study of patients with hemiplegia. Brain 1935;58:448–455.
20.
Sturup G, Bolton B, Williams DJ, Carmichael EA: Vasomotor responses in hemiplegic patients. Brain 1935;58:456–469.
21.
Gardner AW, Killewich LA, Katzel LI, et al: Relationship between free-living daily physical activity and peripheral circulation in patients with intermittent claudication. Angiology 1999;50:289–297.
22.
Bucy PC: Vasomotor changes associated with paralysis of cerebral origin. Arch Neurol Psychiatry 1935;33:30–52.
23.
Herbaut AG, Cole JD, Sedgwick EM: A cerebral hemisphere influence on cutaneous vasomotor reflexes in humans. J Neurol Neurosurg Psychiatry 1990;53:118–120.
24.
Wallin BG, Stjernberg L: Sympathetic activity in man after spinal cord injury: Outflow to skin below the lesion. Brain 1984;107:183–198.
25.
Veldman PHJ, Reynen HM, Arntz IE, Jan R, Goris A: Signs and symptoms of reflex sympathetic dystrophy: Prospective study of 829 patients. Lancet 1993;342:1012–1016.
26.
Bevan R, Clemenson A, Joyce E, Bevan J: Sympathetic denervation of resistance arteries increases contraction and decreases relaxation to flow. Am J Physiol 1993;264:H490–H494.
27.
Bowden REM, Gutman E: Thickening of artery walls and obliteration of capillaries by connective tissue proliferation. Brain 1944;67:273.
28.
Edstrom L, Nystrom B: Histochemical types and sizes of fibers in normal human muscles. Acta Neurol Scand 1969;45:257–269.
29.
Davis ME, Cai H, Drummond GR, Harrison DG: Shear stress regulates endothelial nitric oxide synthase expression through c-Src by divergent signaling pathways. Circ Res 2001;89:1073–1080.
30.
Jondeau G, Katz SD, Zohman LR, Goldberger M, McCarthy M, Boudarias JP, LeJemtel TH: Active skeletal muscle mass and cardiopulmonary reserve: Failure to attain peak aerobic capacity during maximal exercise in patients with congestive heart failure. Circulation 1992;86:1351–1356.
31.
LeJemtel TH, Maskin CS, Lucido D, Chadwick BJ: Failure to augment maximal blood flow in response to one-leg versus two-leg exercise in patients with congestive heart failure. Circulation 1986;74:245–251.
32.
Kernan WN, Inzucchi SE, Viscoli CM, Brass LM, Bravata DM, Shulman GI, McVeety JC, Horwitz RI: Impaired insulin sensitivity among nondiabetic patients with a recent TIA or ischemic stroke. Neurology 2003;60:1447–1451.
33.
Williams GR, Jiang JG, Matchar DB, Samsa GP: Incidence and occurrence of total (first ever and recurrent) stroke. Stroke 1999;30:2523–2528.
34.
Antiplatelet Trialists’ Collaboration: Secondary prevention of vascular disease by prolonged antiplatelet treatment. Br Med J 1988;296:320–331.
35.
Sacco RL, Wolf PA, Kannel WB, McNamara PM: Survival and recurrence following stroke. Stroke 1982;13:290–295.
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
You do not currently have access to this content.