Cervical Spinal Cord Transection Research Articles

Daily variations in the formation of gastric ulcers caused by cervical cord transection in the rat

Cervical spinal cord transection is used as a model of mammalian stress ulcerogenesis. Circadian variations in gastric ulceration have been demonstrated in other animal models. We investigated whether gastric ulceration changed after cervical cord transection throughout a 24-h period by subjecting different groups of rats to cord transection. Ulcers were quantitated using an index described by Szabo and colleagues. Ulcer formation showed significant variation as a function of time of lesioning, with least severe ulceration at 8 AM. We found that cord transection, like other models of gastric ulceration, is also influenced by the circadian system.

Vascular effects of clonidine in patients with tetraplegia and unilateral brachial plexus injury.

Evidence from studies in both animals and in tetraplegics with complete cervical spinal cord transection and preganglionic lesion, indicates that clonidine lowers blood pressure predominantly by a centrally mediated action. We have investigated the haemodynamic basis of this action and performed additional studies in patients with unilateral brachial plexus injury and postganglionic lesions, to further determine the site and mechanism of its action. Blood pressure fell after clonidine in normal subjects but not in tetraplegics. In normal subjects, the fall in blood pressure was associated with a fall in cardiac output, due to a fall in both heart rate and stroke volume. Digital skin vasodilatation occurred after clonidine in normal subjects and only in the innervated limb in patients with unilateral brachial plexus injury. In tetraplegics and in the denervated limb in unilateral brachial plexus injury, there was no vasodilatation; instead a vasoconstrictor response occurred, due to the peripheral adrenoceptor action of clonidine. We conclude that the fall in blood pressure and cardiac output in normal subjects after clonidine were due to its central sympatholytic action. Digital skin vasodilatation after clonidine in normal subjects and the innervated limb in unilateral brachial plexus injury was due to the withdrawal of vasoconstrictor tone and requires intact descending sympathetic pathways.

Effect of intravenous 5-hydroxytryptophan on hypothalamic concentration of norepinephrine, dopamine, serotonin and hydroxyindole acetic acid in the fetal lamb

To investigate the neurochemical mechanism of the response of growth hormone to 5-hydroxytryptophan (5-HTP), we administered 5-HTP (20 mg/kg) to 10 ovine fetuses (110 or 130 days old; term gestation 147 days). Ninety minutes after 5-HTP administration, and following increases in plasma growth hormone concentrations, the fetus was delivered by hysterotomy. After local anesthesia of the fetus and sacrifice by cervical spinal cord transection the hypothalamus rapidly dissected, and stored at −80°C for later analysis of norepinephrine, dopamine, serotonin and hydroxyindole acetic acid. Compared to the administration of saline, 5-HTP caused a significant increase in the hypothalamic content of serotonin, and norepinephrine, at both gestational ages. 5-hydroxyindole acetic acid increased significantly only in the older fetuses. These results indicate that serotonin may not be the only neurotransmitter active in the growth hormone response to 5-HTP.

The Metabolic Impact of Autonomic Neuropathy in Insulin-Dependent Diabetes Mellitus

Long recognized as a cause of cardiovascular and gastrointestinal and genitourinary tract dysfunctions in patients with diabetes mellitus, there is substantial evidence that diabetic autonomic neuropathy plays a fundamental role in the pathogenesis of two clinical metabolic syndromes in patients with diabetes mellitus: hypoglycemia unawareness and defective glucose counterregulation.^1-3 Hypoglycemia unawareness is clearly a neurologic syndrome. It is characterized by the absence of warning symptoms such as sweating, palpitations, and arousal with a decline in the plasma glucose concentration, resulting in neuroglycopenia as the initial and only manifestation of hypoglycemia. Its prototype occurs during experimental hypoglycemia in patients who have suffered cervical spinal cord transections. In patients with diabetes mellitus, hypoglycemia unawareness is associated with, and probably results from, a deficient sympathochromaffin response to plasma glucose decrements.⁴It is generally thought that the absence of warning symptoms increases the frequency of severe iatrogenic hypoglycemia in patients with hypoglycemia

Role of the Central Nervous System in Human Secondary Hypertension

The central nervous system may initiate or maintain hypertension in humans by a variety of mechanisms. Increased cerebral pressor activity can cause hypertension in some patients with the Guillain-Barré syndrome, where disinhibition of cerebral centres may result from an afferent baroreflex lesion. The brain itself initiates hypertension in patients with cerebral tumours, cerebrovascular accidents, and subarachnoid haemorrhage. The use of drugs (including alcohol), or at times their withdrawal, results in hypertension through neurogenic mechanisms. Impaired cerebral activity also contributes, as in tetraplegic patients in whom paroxysmal hypertension is a consequence of increased spinal sympathetic reflex activity, which is not restrained or appropriately counteracted by the brain because of the cervical spinal cord transection. Neurogenic factors also play a role in the maintenance of hypertension in patients in whom the initiating cause is clearly humoral. In renal artery stenosis for instance, cerebral actions of angiotensin II may later gain ascendance over its peripheral effects, especially as circulating levels fall, as has been demonstrated with the centrally acting sympatholytic agent, clonidine. This is an example of humoroneural coupling that contributes to the hypertension. Increased afferent renal nerve activity may be an additional factor, especially in patients with renal parenchymal disease, where renin appears to play a minor role. The role of the nervous system in other causes of primary hypertension is presently less clear. In phaeochromocytoma noncatecholamine tumour products may have neurogenic effects that could account for the ability of clonidine to lower blood pressure in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood flow in skeletal muscle of tetraplegic man during postural changes.

Relative changes in blood flow and vascular resistance in arm and leg muscle during head-up tilt at 45 degrees were studied in eight patients with complete cervical spinal cord transection and in 13 healthy volunteers. Muscle blood flow was measured by the local 133Xe washout method. In forearm muscle kept at heart level blood flow remained constant in the tetraplegic patients during head-up tilt, in contrast to that seen in the normal subjects, where blood flow decreased by 30%. In the dependent leg muscle, head-up tilt caused a decrease in blood flow of 46% and 40% in the patients and normals, respectively. Abolition of the local veno-arteriolar axon reflex, by inducing local counter-pressure to prevent venous distension in the dependent leg muscle, reduced the decrease in blood flow to 24% and 23%, respectively. Thus, the vascular response to head-up tilt differed significantly in forearm muscle between the two groups, whereas no difference was seen in the leg muscle. The absence of the vasoconstrictor response in forearm muscle indicates that postural sympathetic reflexes to this region depend on sympathetic reflexes integrated in centres located rostrally to the spinal cord. The results further suggest that local veno-arteriolar axon reflexes as well as spinal reflexes contribute to the observed vasoconstriction in the leg muscle.

Electrophysiological and morphological correlates of axotomy-induced deafferentation of the goldfish Mauthner cell.

Axotomy-induced changes in afferent synapses to the goldfish Mauthner cell have been analyzed with intracellular recordings and with electron microscopy. The studies encompassed 7-208 days after cervical spinal cord transection. The physiological findings suggest a persistent and specific reduction in excitatory chemical inputs to the soma and proximal lateral dendrite, with no changes in somatic inhibition or in the electrotonic and chemical inputs to the more distal regions of the lateral dendrite. Corroborative morphological evidence includes swelling of the M-cell soma, as indicated by a 35% increase in the length of its minor diameter, an increased spacing and a quantitatively lower density of terminals on the soma, and the appearance of astrocytic processes partially or completely engulfing the terminals in that region. Similar changes were observed on the inferior dendrites projecting from the ventral surface of the soma, although these dendrites do not exhibit the chromatolytic changes observed at the soma. In contrast, there are no noticeable changes in either the synaptic investment of the lateral dendrite or its ultrastructure. Quantitative and qualitative data support the conclusion that there is a restricted and specific reduction in the proximal excitatory inputs to the M-cell. The evidence also suggests that electrotonic junctions between afferents and the M-cell remain intact, functionally and structurally.

Respiratory responses to ventilatory loading following low cervical spinal cord injury.

This study compared the respiratory responses to ventilatory loading in 8 normal subjects and 11 quadriplegic patients with low cervical spinal cord transection. Progressive hypercapnia was produced by rebreathing. Rebreathing trials were carried out with no added load and with inspiratory resistive loads of 5 and 16 cmH2O. l-1 X s. Measurements were made of ventilation and of diaphragmatic electromyographic activity. Base-line hypercapnic ventilatory responses were significantly lower than normal in the quadriplegic patients, but the effects of resistive loading on the ventilatory responses were comparable in the two groups. The change in peak moving-average diaphragmatic electrical activity (DI peak) for a given change in CO2 partial pressure (PCO2) and DI peak at PCO2 55 Torr increased significantly with resistive loading both in the normal subjects and the quadriplegic patients. In the normal subjects, but not in the quadriplegic patients, inspiratory duration increased progressively with increasing resistance. The increase in DI peak during ventilatory loading in the normal subjects was a consequence of inspiratory prolongation. In contrast, in the quadriplegic patients during breathing against the larger resistive load, there was a significant increase in the average rate of rise (DI peak divided by the time from onset to peak) of diaphragmatic activity. The change in DI rate of rise for a given change in PCO2 increased to 137 +/- 13% (SE), and the DI rate of rise at PCO2 55 Torr increased to 128 +/- 8% (SE) of control values. These results indicate that compensatory increases in diaphragmatic activation during ventilatory loading occur in quadriplegic patients in whom afferent feedback from rib cage receptors is disrupted.

Brain and lungs at risk after cervical spinal cord transection: Intracranial pressure, brain water, blood-brain barrier permeability, cerebral blood flow, and extravascular lung water changes

The early physiopathologic responses to transection of the cervical spinal cord (C-4) were studied in the experimental animal. After transection, increases were seen in the mean arterial pressure, pulmonary capillary wedge pressure, intracranial pressure, brain water, blood-brain barrier permeability, and extravascular lung water with a marked decrease occurring in cerebral blood flow. Pretreatment with an α-adrenergic blocker, phentolamine (Regitine Ciba-Geigy Corp.), followed by transection blocked the rise in mean arterial blood pressure and pulmonary capillary wedge pressure but did not affect the increases in intracranial pressure, brain water, blood-brain barrier permeability, and extravascular lung water and decreases in cerebral blood flow. Transection of the cervical spinal cord initiates a complex series of events involving intracranial compliance and pulmonary permeability, placing both brain and lungs at risk.

Splenic, renal, and cardiac nerves have unequal dependence upon tonic supraspinal inputs

Stimulation of visceral receptors can lead to unequal reflex responses in splenic, renal and cardiac sympathetic nerves. Activity of splenic nerves is often more excited or less inhibited than that of cardiac or renal nerves. This study was undertaken to determine potential differences in resting discharge among these 3 nerves. Dependence upon supraspinal drive was evaluated by comparing the relative decrease in activity of these nerves in chloralose-anesthetized cats 30 min to 2 h following high cervical spinal cord transection. After this transection, discharge rates of cardiac and renal nerves were significantly depressed to less than 50% of initial values. In contrast, splenic nerve activity was not significantly affected. To determine if this sustained splenic nerve activity resulted from greater responsiveness to potential external sources of excitation, splenic, renal and cardiac neural responses to factors known to affect sympathetic discharge in spinal animals were compared. Neither increased arterial pressure, decreased arterial pressure, systemic hypercapnia and acidosis, nor thoracolumbar dorsal rhizotomy revealed specific inputs responsible for the preferential maintenance of splenic nerve activity in spinal cats. It was concluded that ongoing activity of splenic nerves is less dependent upon supraspinal sources of excitation than is activity of renal or cardiac nerves. The cause of this difference among these 3 components of sympathetic outflow remains to be determined.

Cholecystokinin-induced excitation in the substantia nigra: evidence for peripheral and central components

Cholecystokinin (CCK), one of the most common brain peptides, coexists with dopamine (DA) in neurons of the medial substantia nigra (SN). CCK has been shown to excite these neurons following either direct iontophoretic or systemic administration suggesting that peripherally administered CCK may cross the blood brain barrier to act directly on nigral DA cells. However, biochemical evidence suggests that CCK does not cross the blood brain barrier, and several studies have shown that the behavioral and the satiety-inducing effects of peripherally administered CCK are abolished by vagotomy. In order to test for vagal mediation of the nigral response to systemically administered CCK, we examined the effects of a series of lesions to the vagal pathways on CCK-induced excitation in the SN. Neither acute thoracic nor chronic subdiaphragmatic vagotomies had any effect on the excitatory response of nigral DA neurons to systemically administered CCK. High cervical spinal cord transections were similarly without effect. In contrast, lesions of either vagal fibers in the medulla or of the efferent pathways from the nucleus tractus solitarii, the primary sensory nucleus of the vagus, produced significant attenuations of the nigral effects of systemically administered CCK. However, neither lesion blocked effects of CCK completely. We suggest that peripherally administered CCK has two components to its excitatory action in the SN; a component probably mediated through CCK receptors in the nucleus tractus solitarii and a direct action on DA neurons.

Substance P mechanisms of the spinal cord related to vasomotor tone in the spontaneously hypertensive rat

This report deals with substance P (SP) mechanisms involved in regulation of vasomotor tone at the spinal cord levels in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Our results indicate the following. (1) Intrathecal injections of the SP antagonist, d-Pro 4, d-Trp 7.9-SP 4–11 cause dose-dependent decreases in mean arterial pressure and heart rate in Sprague-Dawley rats, WKYs and SHRs; the maximal blood pressure decreases are equal to those seen after cervical spinal cord transection. (2) Intrathecal injections of this antagonist into the L1 spinal level in WKYs or SHRs that had previously had their C8 spinal cords transected caused a rise in blood pressure and heart rate, suggesting that intrinsic spinal SP mechanisms are probably not involved in vasomotor tone. (3) The intermediolateral cell column region (IML) of 16-week-old WKYs and SHRs has a single high affinity and saturable binding component with approximately the same dissociation constant ( K d = 1.21nM for WKYs; K d = 1.25nM for SHRs); the SHRs showed a higher number of sites (B max= 24.5fmol/mg protein) than WKY rats (B max= 19.9fmol/mg protein). The K d and B max obtained from IML sections from 4-week-old WKYs and SHRs exhibit no differences, although their binding values with 2 nM [ 3H]SP are higher than those obtained from the 16-week-old animals. (4) d-Pro 4, d-Trp 7,9-SP 4–11 has the same relatively low (micromolar range) potency for displacing [ 3H]SP binding in the IML of WKYs and SHRs ((5) SHRs (16 weeks old) contain 20% more SP immunoreactivity in the IML than WKY rats (834 ± 36pg/mg protein vs694 ± 50pg/mg protein); 4-week-old rats do not show such differences. The potential significance of these results is discussed in relation to the control of vasomotor tone.

Cardiovascular responses elicited by microinjection of monoamines into mesencephalic nucleus dorsalis raphe in cats.

The effect of monoaminergic agonists and antagonists microinjected into mesencephalic nucleus dorsalis raphe has been studied on blood pressure and heart rate to elucidate the nature and role of these monoaminergic receptors in cardiovascular regulation. Microinjection of monoamines, noradrenaline, phenylephrine and 5-hydroxytryptamine (5-HT) into nucleus dorsalis raphe elicited hypertension and tachycardia which could be blocked by local pretreatment with piperoxan (an alpha-adrenoceptor blocker) and methysergide (a 5-HT receptor blocker) respectively. However, isoprenaline microinjections failed to evoke any response. Bilateral vagotomy did not prevent these cardiovascular responses evoked by monoamines microinjection, while cervical spinal cord (C1) transection with bilateral vagotomy prevented these responses. These monoaminergic receptors seem to be localized in nucleus dorsalis raphe since microinjection of monoamines into neural structures adjoining nucleus dorsalis raphe, failed to induce any cardiovascular response. Monoaminergic receptors are present in nucleus dorsalis raphe which modulate cardiovascular activity by influencing sympathetic preganglionic neurons in the intermediolateral columns of the spinal cord.

家兎脳底槽内への薬剤注入による心電図の変化

Abnormalities in ECG frequently occurring in patients associated with cerebrovascular lesions, especially subarachnoid hemorrhage, have been documented in many reports. Similar abnormalities in ECG have also been reported on such experiments as following electric stimulation of various sites of the brain, direct intracranial injection of space taking substances or induced ICP elevation.Drugs are currently administered commonly by injection into the cisterna magna o r via the transorbital approach, however approach to the circle of Willis is difficult by either method or hemorrhage due to puncture of adjacent vessels may frequently occur. The author produced in rabbits a method injecting small amounts of drugs via the craniopharyngeal duct into the basal cistern with reduced surgical damage and minimal influences on the systemic circulation.1. Direct administration of 0.5ml or less of physiological saline into the basal cistern of the rabbit via craniopharyngeal duct produced no changes in the systemic circulation or ECG.2. Withdrawal of 1.0ml of cerebrospinal fluid from the craniopharyngeal duct and subsequent injection of serotonin (10mg-1.0ml) induced no changes in ECG except bradycardia.3. When prostaglandin F2α (500pg-0.5ml) was injected into the basal cistern, supraventricular and ventricular arrhythmia were observed in ECG after a mean interval of 301sec. ± 74sec., and S-T depression and lower T wave remained for more than 45 minutes. An increase i n blood pressure and a decrease in the heart rate were also noted.4. Intravenous administration of the same dose of PGF2a caused no changes in ECG except bradycardia.5. Injection of the same dose into the basal cistern after cervical spinal cord transection at the C2-C3 level induced no changes in ECG.6. Thus the stimulation by the injection of PGF2a was shown to be conducted down to the heart via the cervical spinal cord.7. A decrease in PaCO2 was observed following injections of serotonin or PGF2α into the basal cistern.

Neurological analysis of respiratory, cardiovascular and neuromuscular effects of brevetoxin in cats

H. L. Borison, L. E. McCarthy and S. Ellis. Neurological analysis of respiratory, cardiovascular and neuromuscular effects of brevetoxin in cats. Toxicon 23, 517 – 524, 1985. — Effects of brevetoxin were evaluated in cats anesthetized with pentobarbital under conditions of controlled end-expiratory pCO 2 and constant body temperature. Recordings were made of arterial blood pressure, heart rate, respiratory pattern, diaphragm EMC, evoked tibialis muscle twitch and evoked contraction of the nictitating membrane. Electrical stimulation was employed for periodic excitation of the medullary respiratory center, the phrenic nerve, the peroneal nerve and the cervical sympathetic nerve. Brevetoxin was prepared at a concentration of 1.0 mg/ml in an aqueous medium of 2.5% ethanol plus 2.5% Emulphor 620 (General Aniline and Film Corp., New York). Small i.v. bolus injections of the toxin (40 μ/kg) evoked, without tachyphylaxis, the Bezold - Jarisch reflex triad of bradycardia, hypotension and bradypnea. This effect was essentially abolished by vagotomy. Continued injections then resulted in pressor reactions and tachycardia, along with the development of respiratory dysrhythmia. Large doses of brevetoxin (160 μ/kg i.v.) caused somatomotor seizures accompanied by severe hypertension, that occurred even after decerebration and cervical spinal cord transection. Cranial intra-arterial and intra-cerebroventricular injections of brevetoxin produced hypertension and respiratory depression more effectively than did i.v. injections. Systemic cumulation of the toxin, with the respiration supported artificially, caused death from cardiovascular collapse, without significant blockade of neuromuscular and ganglionic transmission. It is concluded that brevetoxin exerts its major toxic effects on the circulation and respiration through reflex and central actions, largely sparing peripheral motor mechanisms.

Sensation of respiratory force following low cervical spinal cord transection.

The psychophysical technique of magnitude scaling was used to assess the sensation of respiratory muscle force in patients with low cervical spinal cord transection. The exponents of the power function relationship between load magnitude and sensation intensity during graded elastic and resistive ventilatory loading in the quadriplegic patients were 0.51 and 0.54, respectively. These values were significantly lower than those in normal subjects (P less than 0.05). This impairment in load sensation could not be attributed to differences in either the duration or magnitude of the forces generated by muscles of inspiration during loading, since the power function relationships between airway pressure and sensation intensity corrected for inspiratory duration were also significantly lower in the quadriplegic patients compared with the normal subjects. In contrast the perception of respiratory force during inspiratory maneuvers against a closed airway, as determined by both magnitude estimation and production tests, was the same in normal subjects and quadriplegics. These results suggest that afferent signals from rib cage receptors are important in shaping the intensity of the sensation during submaximal ventilatory loading. During maximal loading, i.e., airway occlusion, when respiratory muscle tension changes proportionally with the motor command, centrally generated efferent command signals may be employed to subserve the sensation of respiratory muscle force when inputs from rib cage muscle receptors are not available.

Blockade of GABA receptors in periventricular forebrain of anesthetized cats: Effects on heart rate, arterial pressure, and hindlimb vascular resistance

Pharmacologic antagonism of GABAergic inhibition in the periventricular forebrain of anesthetized cats caused dose related (1) sympathetically mediated increases in heart rate and arterial pressure in vagotomized cats, and (2) suppression of reflex vagal activation in vagus-intact preparations where sympathetic effects are prevented by cervical spinal cord transection. In the present study performed in cats with intact autonomic pathways, similar administration of the GABA antagonist bicuculline methiodide (BMI) produced dose-related increases in arterial pressure, heart rate, and, when perfusion pressure in the autoperfused hindlimb was measured, vascular resistance. Furthermore, the relationship between heart rate and hindlimb vascular resistance changes suggested that the effects on heart rate reflected the combined sympathetic and vagal baroreflex effects of BMI. Intraventricular administration of muscimol, a potent GABA agonist, elicited abrupt and parallel reversal of BMI-induced effects on systemic arterial pressure and vascular resistance while attempts to acutely denervate the hindlimb at the height of the BMI response by cutting the femoral and sciatic nerves sharply reversed the increase in hindlimb vascular resistance in most experiments. The results suggest that the cardiovascular changes observed represent an integrated pattern consisting of excitation of sympathetic nerves innervating the heart and vasculature along with suppression of reflex evoked vagal excitability.

Inhibitory influences from arterial baroreceptors on vasopressin release elicited by fastigial stimulation in rats.

Electrical stimulation of the fastigial nucleus in anesthetized, paralyzed, and artificially ventilated rats for 10 seconds (50 Hz) induced a stimulus-locked elevation of arterial pressure (the fastigial pressor response) and increased plasma vasopressin. Cervical spinal cord transection abolished the stimulus-locked fastigial pressor response and augmented the vasopressin response to a 10-fold increase (19 +/- 1 to 188 +/- 58 pg/ml, P less than 0.05; n = 8). Grading the pressor elevations occurring during the fastigial nucleus stimulus changed the amounts of vasopressin released in the same animal: acute adrenalectomy and chemosympathectomy by guanethidine reduced the magnitude of the fastigial pressor response and facilitated the vasopressin release to fastigial nucleus stimulation (intact: 52 +/- 11 pg/ml; after adrenalectomy and chemosympathectomy, 254 +/- 73 pg/ml, P less than 0.05, n = 6). Subsequent intravenous administration of a bolus of phenylephrine to increase mean arterial pressure during fastigial nucleus stimulus, as in intact situation, reduced the vasopressin release (47 +/- 9 pg/ml). After sinoaortic denervation plus vagotomy, the fastigial pressor response was preserved; however, vasopressin still increased 11-fold (from 11 +/- 1 to 126 +/- 23 pg/ml, P less than 0.01, n = 8). Vagotomy alone did not affect the vasopressin resting level nor the 4-fold increase in response to fastigial nucleus stimulation. Therefore, stimulus-locked elevations of arterial pressure oppose, by reflex mechanisms mediated through baroreceptors, but do not prevent the release of vasopressin elicited by stimulation of the fastigial nucleus.

Multisegmental spinal sympathetic reflexes originating from the heart.

Activation of cardiac sympathetic afferent nerves can initiate excitatory cardiocardiac reflexes through pathways that are exclusively spinal. In addition, stimulation of the same nerves also causes lower thoracic and lumbar sympathetic excitation, but the contribution of spinal pathways to these reflexes is unknown. Therefore experiments were performed to compare cardiac, splenic, and renal sympathetic responses to cardiac sympathetic afferent stimulation before and after cervical spinal cord transection in anesthetized, vagotomized, sinoaortic-denervated cats. Electrical stimulation of afferent cardiac sympathetic nerves produced excitatory responses in cardiac and renal nerves before transection but only cardiac nerve responses after transection. In contrast, afferent stimulation by epicardially applied bradykinin excited cardiac, renal, and splenic nerves before and after cord transection. Splenic nerve responses were greater than renal nerve responses in intact and spinal cats. These results demonstrate that spinal reflexes initiated by activation of cardiac sympathetic afferent nerves are not limited to cardiocardiac pathways. The similarity of patterns of responses in intact and spinal cats suggests that spinal pathways contribute significantly to the reflex excitation observed in intact animals.

Clinical manifestations of malfunctioning sympathetic mechanisms in tetraplegia

Patients who are tetraplegic with cervical spinal cord transection do not appear to have cerebral control over the sympathetic nervous system. Soon after transection they are often in a state of spinal shock during which even isolated spinal cord sympathetic activity is absent. This affects, in particular, the cardiovascular system and other homeostatic mechanisms which are dependent on appropriate regulation of the vasculature, such as thermoregulation. After a few weeks isolated spinal cord activity returns but the absence of control by the brain results in sympathetic malfunction of various systems. Inappropriate inactivity therefore occurs during postural change and causes orthostatic hypotension, while over-activity, which results in the syndrome of autonomic dysreflexia and hypertension, occurs if spinal sympathetic reflexes are activated. Examples are provided of clinical effects of sympathetic malfunction in tetraplegics in relation to circulatory, thermoregulatory, pupillary, genital, gastrointestinal and urinary tract function.