Input–output relationships of a somatosympathetic reflex in human spinal injury

Brown, Rebecca; Burton, Amy L.; Macefield, Vaughan G.

doi:10.1007/s10286-009-0010-9

Cited by 11 publications

(15 citation statements)

References 27 publications

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“…While each of these studies found that a complete spinal lesion abolishes sudomotor responses in the lower limbs to electrical stimulation above lesion, Cariga et al (2002) concluded that the isolated spinal cord cannot generate cutaneous sympathetic responses, as demonstrated by the absence of electrodermal responses in the lower limbs to stimuli delivered below lesion. While sudomotor responses to electrical stimulation below the lesion have occasionally been found (Fuhrer, 1975; Reitz et al, 2003), in our experience sudomotor responses in SCI are very unreliable markers of increases in cutaneous sympathetic outflow (Brown et al, 2007, 2009a,b; Brown and Macefield, 2008). …”

Section: Assessing Sympathetic Outflow Below Lesion Following Human Smentioning

confidence: 49%

Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

Macefield¹,

Burton²,

Brown³

2012

Front. Physio.

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It is known that the sudden increases in blood pressure associated with autonomic dysreflexia in people with spinal cord injury (SCI) are due to a spinally mediated reflex activation of sympathetic vasoconstrictor neurons supplying skeletal muscle and the gut. Apart from visceral inputs, such as those originating from a distended bladder, there is a prevailing opinion that autonomic dysreflexia can be triggered by noxious stimulation below the lesion. However, do noxious inputs really cause an increase in blood pressure in SCI? Using microelectrodes inserted into a peripheral nerve to record sympathetic nerve activity we had previously shown that selective stimulation of small-diameter afferents in muscle or skin, induced by bolus injection of hypertonic saline into the tibialis anterior muscle or the overlying skin, evokes a sustained increase in muscle sympathetic nerve activity and blood pressure and a transient increase in skin sympathetic nerve activity and decrease in skin blood flow in able-bodied subjects. We postulated that these sympathetic responses would be exaggerated in SCI, with a purely noxious stimulus causing long-lasting increases in blood pressure and long-lasting decreases in skin blood flow. Surprisingly, though, we found that intramuscular or subcutaneous injection of hypertonic saline into the leg caused negligible changes in these parameters. Conversely, weak electrical stimulation over the abdominal wall, which in able-bodied subjects is not painful and activates large-diameter cutaneous afferents, caused a marked increase in blood pressure in SCI but not in able-bodied subjects. This suggests that it is activation of large-diameter somatic afferents, not small-diameter afferents, that triggers increases in sympathetic outflow in SCI. Whether the responses to activation of large-diameter afferents reflect plastic changes in the spinal cord in SCI is unknown.

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Section: Assessing Sympathetic Outflow Below Lesion Following Human Smentioning

confidence: 49%

Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

Macefield¹,

Burton²,

Brown³

2012

Front. Physio.

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“…Waveform averages of SNA or dorsal root potentials (DRPs) to 50 cycles of SN or TN stimulation (0.2 ms duration, 1-80 V, 0.5, or 1 Hz) were generated. Voltage intensity was increased incrementally from 1 V (subthreshold) to 80 V (supramaximal) at intervals: 1,2,4,6,8,10,12,15,20,25,30,40,50,60, 80 V, and the stimulus was repeated twice at each voltage. The threshold voltage for SSR responses was ϳ3-4 V. Stimulus intensities between 4 and 12 V activated A-fiber afferents and were classed as low intensity; Ͼ 30 V activated A-and C-fiber afferents and was classed as high intensity (see Fig.…”

Section: Electrophysiological Experimentsmentioning

confidence: 99%

“…Sympathetic activation generated by SSR originates from both spinal and supraspinal levels (4,45). In anesthetized animals, the shortlatency spinal SSR is rarely observed due to tonic suppression by descending supraspinal inputs from several sources, including the RVLM and A5 and A6 regions (10,11,19,55).…”

mentioning

confidence: 99%

Patterning of somatosympathetic reflexes reveals nonuniform organization of presympathetic drive from C1 and non-C1 RVLM neurons

Burke

Neale

Korim

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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To determine the organization of presympathetic vasomotor drive by phenotypic populations of rostral ventrolateral medulla (RVLM) neurons, we examined the somatosympathetic reflex (SSR) evoked in four sympathetic nerves together with selective lesions of RVLM presympathetic neurons. Urethane-anesthetized (1.3 g/kg ip), paralyzed, vagotomized and artificially ventilated Sprague-Dawley rats (n = 41) were used. First, we determined the afferent inputs activated by sciatic nerve (SN) stimulation at graded stimulus intensities (50 sweeps at 0.5-1 Hz, 1-80 V). Second, we recorded sympathetic nerve responses (cervical, renal, splanchnic, and lumbar) to intensities of SN stimulation that activated A-fiber afferents (low) or both A- and C-fiber afferents (high). Third, with low-intensity SN stimulation, we examined the cervical SSR following RVLM microinjection of somatostatin, and we determined the splanchnic SSR in rats in which presympathetic C1 neurons were lesioned following intraspinal injections of anti-dopamine-β-hydroxylase-saporin (anti-DβH-SAP). Low-intensity SN stimulation activated A-fiber afferents and evoked biphasic responses in the renal, splanchnic, and lumbar nerves and a single peak in the cervical nerve. Depletion of presympathetic C1 neurons (59 ± 4% tyrosine hydroxylase immunoreactivity profiles lesioned) eliminated peak 2 of the splanchnic SSR and attenuated peak 1, suggesting that only RVLM neurons with fast axonal conduction were spared. RVLM injections of somatostatin abolished the single early peak of cervical SSR confirming that RVLM neurons with fast axonal conduction were inhibited by somatostatin. It is concluded that unmyelinated RVLM presympathetic neurons, presumed to be all C1, innervate splanchnic, renal, and lumbar but not cervical sympathetic outflows, whereas myelinated C1 and non-C1 RVLM neurons innervate all sympathetic outflows examined. These findings suggest that multiple levels of neural control of vasomotor tone exist; myelinated populations may set baseline tone, while unmyelinated neurons may be recruited to provide actions at specific vascular beds in response to distinct stressors.

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“…In the absence of central modulation, reflexly evoked vasoconstriction elicited by distension of visceral organs, or by some other unheeded afferent input from caudal to the lesion, is exaggerated (21). In SCI patients, spinal reflex-evoked vasoconstriction is most readily studied in the skin (e.g., 7,8,34), where modified neural control of blood flow results in poor thermoregulation (21) and may contribute to increasing the risk of pressure sores and impair wound healing (11,37).…”

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confidence: 98%

Prominent contribution of L-type Ca²⁺channels to cutaneous neurovascular transmission that is revealed after spinal cord injury augments vasoconstriction

Dera¹,

Habgood

Furness³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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In patients with spinal cord injury (SCI), somatosympathetic reflexes produce exaggerated decreases in skin blood flow below the lesion. This hypoperfusion appears to result from an increased responsiveness of cutaneous arterial vessels to neural activation. Here we investigated the mechanisms that underlie SCI-induced enhancement of neurovascular transmission in a cutaneous vessel, the rat tail artery. Isometric contractions of arterial segments from T11 spinal cord transected and sham-operated rats were compared 6 wk postoperatively. SCI more than doubled the amplitudes of contractions of arteries in response to moderate frequencies of nerve stimulation (0.1 to 1 Hz). In arteries from SCI rats, but not those from sham-operated rats, the L-type Ca(2+) channel blocker nifedipine (1 μM) reduced the amplitudes of nerve-evoked contractions. Furthermore, while the sensitivity to the agonists phenylephrine (α(1)-adrenoceptor selective) and clonidine (α(2)-adrenoceptor selective) did not differ significantly between arteries from SCI and sham-operated rats, nifedipine had a greater inhibitory effect on contractions to both agents in arteries from SCI rats. Although sensitivity to clonidine was unchanged, SCI selectively reduced the contribution of postjunctional α(2)-adenceptors to nerve-evoked contractions. In arteries from unoperated rats, the L-type channel agonist BAY K 8644 (0.1 μM) produced a similar enhancement of nerve-evoked contraction to that produced by SCI and also selectively reduced the contribution of α(2)-adrenceptors to these responses. Together the findings demonstrate that the SCI-induced enhancement of neurovascular transmission in the rat tail artery can largely be accounted for by an increased contribution of L-type Ca(2+) channels to activation of the vascular smooth muscle.

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Input–output relationships of a somatosympathetic reflex in human spinal injury

Abstract: We conclude that there is a non-linear relationship between somatic inputs and sympathetic vasoconstrictor outputs, and argue that a sustained vasoconstriction need not imply continuous sensory input to the spinal cord.

Cited by 11 publications

References 27 publications

Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

Patterning of somatosympathetic reflexes reveals nonuniform organization of presympathetic drive from C1 and non-C1 RVLM neurons

Prominent contribution of L-type Ca²⁺channels to cutaneous neurovascular transmission that is revealed after spinal cord injury augments vasoconstriction

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Input–output relationships of a somatosympathetic reflex in human spinal injury

Abstract: We conclude that there is a non-linear relationship between somatic inputs and sympathetic vasoconstrictor outputs, and argue that a sustained vasoconstriction need not imply continuous sensory input to the spinal cord.

Cited by 11 publications

References 27 publications

Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

Patterning of somatosympathetic reflexes reveals nonuniform organization of presympathetic drive from C1 and non-C1 RVLM neurons

Prominent contribution of L-type Ca2+channels to cutaneous neurovascular transmission that is revealed after spinal cord injury augments vasoconstriction

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Prominent contribution of L-type Ca²⁺channels to cutaneous neurovascular transmission that is revealed after spinal cord injury augments vasoconstriction