Sm. Jespersen et al., 2-LEVEL SPINAL STENOSIS IN MINIPIGS - HEMODYNAMIC-EFFECTS OF EXERCISE, Spine (Philadelphia, Pa. 1976), 20(24), 1995, pp. 2765-2773
Study Design, Twenty-two Gottingen minipigs were trained to run on a t
readmill. Two-level lumbar spinal stenosis was created in 12 pigs, 10
were unoperated control subjects. Blood flow of the spinal cord and ne
rve roots was determined with microspheres at rest, during exercise, a
nd after exercise. Objectives. To study the effect of lumbar spinal st
enosis and exercise on blood flow of spinal neural tissue. Summary of
Background Data. Neurogenic claudication, the key symptom of lumbar sp
inal stenosis, may be caused by vascular impairment or mechanical dist
ress of neural tissue during exercise. Experimental compression of the
cauda equina causes reversible nerve root edema, stasis, blood flow d
ecrease, and compromised neural function. The vascular pathophysiology
of spinal stenosis during exercise: has not been studied previously.
Methods. Pigs were trained daily for 3 months. Two-level 25% lumbar sp
inal stenosis was introduced by placement of stenosing bands around th
e dural sac. Neurologic function was monitored before surgery by evoke
d potentials and after surgery by the Tarlov score, Regional blood flo
w in lumbosacral neural tissue was measured 3 days after chronic cathe
terization using microspheres at rest, during exercise at 3 km/h for 1
5 minutes, and at rest 30 minutes after exerciser. Results. Blood flow
of grey and white matter increased during exercise in both groups, wi
th no differences between groups. Slight hyperemia prevailed after exe
rcise in white matter of the stenotic area but not in grey matter. Ner
ve root blood flow was largely unchanged in control subjects during ex
ercise but was reduced in spinal stenosis at rest, further depressed d
uring exercise, and normalized after exercise. Dural blood flow was el
evated throughout. Conclusions. The study suggests that exercise-induc
ed impairment of spinal nerve root blood flow plays a role in the path
ophysiology of neurogenic claudication.