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[The prediction of atrial fibrillation recurrence after electrical cardioversion with the chemoreflex sensitivity].

UNLABELLED: Patients with paroxysmal atrial fibrillation have a lower chemoreflex sensitivity (CHRS) which is characterized as an autonomic dysfunction. Because of this observation we examined the theory of an autonomic dysfunction as the reason for the reccurrence of atrial fibrilation after electrical cardioversion. METHOD: We measured the CHRS among 43 patients 24 h after successful electrical cardioversion and the patients were controlled for at least 6 months. RESULTS: During the six months of follow-up a recurrence was observed in 18 patients with a mean of 8.3 days. There was no difference in organic heart disease or in the use of drugs. Left atrial diameter was not significantly larger in patients with a recurrence. Patients with a recurrence have a significantly lower CHRS than patients with sinus rhythm (2.41 +/- 1.82 vs 5.62 +/- 3.02 ms/mmHg, p < 0.04). The diagnostic value of a CHRS below 3.0 ms/mmHg achieved a specificity of 68%, a sensitivity of 67%, a positive and negative predictive value of 60% and 74%. CONCLUSIONS: An analysis of CHRS seems to be an appropriate method to predict a recurrence of atrial fibrillation. The predictive power of the method has to be examined by prospective investigations of a larger patient population and a longer follow-up. Patients with paroxysmal atrial fibrillation have a lower chemoreflex sensitivity (CHRS) which is characterized as an autonomic dysfunction. Because of this observation we examined the theory of an autonomic dysfunction as the reason for the recurrence of atrial fibrillation after electrical cardioversion.

Adrenergic beta-Antagonists↗

Autonomic nerve dysfunction in pathologically obese patients.

BACKGROUND: Obese patients frequently present clinical symptoms related to gastrointestinal motility alterations and autonomic nervous system dysfunction. AIM: To evaluate the possible correlation between cardiovascular autonomic nervous dysfunction and oesophageal motility in pathologically obese patients. PATIENTS AND METHODS: Enrolled in the study were 22 patients with a body mass index of 45.72 +/- 7.48 and 10 control subjects, all within 20% of their ideal weight. Oesophageal motility was measured by stationary manometry and scintigraphic transit. Tests for the evaluation of autonomic nervous system were: Valsalva ratio, deep breathing, sustained handgrip, sudormotor axon reflex test and spectral analysis of the variability of R-R interval. RESULTS: The mean pressure of oesophageal peristaltic waves in patients and controls was 39.36 +/- 14 mmHg and 73 +/- 12 mmHg, respectively The scintigraphic mean transit time was 22.96 +/- 16.26 seconds in patients and 10.23 +/- 16.26 seconds in controls (p < 0.001). Spectral analysis of the variability of the R-R interval showed an increase in the parasympathetic component both in the lying and standing position compared to controls. The other autonomic nervous system function tests showed no significant difference between obese patients and controls. CONCLUSIONS: These results suggest that obese patients present a reduction of oesophageal transit and autonomic nervous system dysfunction albeit no direct correlation was found between these phenomena.

Adult↗

[Bioelectrical activity of the brain during 49-day antiorthostatic hypokinesia in persons with the early signs of autonomic vascular dysfunction].

Cerebral bioelectric activity of 18 male test subjects (9 test subjects with early manifestations of autonomic-vascular dysfunctions of the hypertensive, hypotensive or cardiac type, and 9 healthy test subjects), aged 25 to 42, was studied during their 49-day head-down tilting (-4 degrees) and during recovery. On the 5th experimental day their EEG showed signs of CNS irritation and increased excitation in response to photostimulation. That was very marked in the test subjects with autonomic-vascular dysfunctions. On the 15, 30 and particularly 45th experimental day their EEG showed both diffusion and paroxysmal slow activity; CNS excitability decreased significantly during rhythmic photostimulation. By the 20th--22nd day of recovery EEG parameters returned to normal. This indicates that the changes were reversible and that the therapeutic measures applied were effective.

Adult↗

Homocysteine levels are not associated with cardiovascular autonomic function in elderly Caucasian subjects without or with type 2 diabetes mellitus: the Hoorn Study.

OBJECTIVE: Homocysteine and cardiovascular autonomic function are both predictors of cardiovascular disease and death, particularly in patients with diabetes. The mechanism by which homocysteine causes disease is unknown. The objective of our study was to determine whether hyperhomocysteinaemia is associated with impaired cardiovascular autonomic function in an age-, sex-, and glucose tolerance-stratified sample of an elderly Caucasian population. METHODS: We studied 609 subjects, 252 with normal glucose metabolism, 173 with impaired glucose metabolism, and 184 with type 2 diabetes. Cardiac cycle duration (RR interval) and continuous finger arterial pressure were measured under three conditions: during (i) spontaneous breathing, (ii) six deep breaths over 1 min, and (iii) an active change in position from lying to standing. From these readings, 10 parameters of autonomic function were assessed (three Ewing tests, six heart rate variability tests and one test of baroreflex sensitivity). These 10 measurements were summarized in a single cardiovascular autonomic dysfunction score (CADS). RESULTS: Comparing values of autonomic function measures in the lowest versus the highest quartile of homocysteine revealed no significant association between homocysteine level and autonomic function in the whole study group, nor in the individual glucose tolerance groups. Multiple adjustment for age, sex, waist-to-hip ratio, serum creatinine, use of antihypertensives and fasting insulin, confirmed this result. We found no evidence of effect modification of glucose tolerance status on the association between homocysteine and autonomic dysfunction (P for interaction for CADS = 0.79). CONCLUSIONS: There is no evidence for an association between homocysteine levels and cardiovascular autonomic function in either diabetic or nondiabetic subjects. Cardiovascular autonomic dysfunction does not help explain why hyperhomocysteinaemia is related to cardiovascular mortality.

Age Factors↗

Modulation of host immunity by HIV may be partly achieved through usurping host autonomic functions.

Modulation of host immunity has been observed in human immunodeficiency virus (HIV) infections. HIV is believed to influence host immunity through a variety of mechanisms including direct effects on host T cell survival, indirect effects on cytokine profile through modulation of immune cells, and modulation of endocrine functions that affect immunity such as steroids. We hypothesize that HIV infection may also alter host immunity through modulation of host sympatho-vagal balance. Specifically, we propose that HIV drives autonomic balance towards sympathetic bias, which can contribute to a T helper (Th)2 type immunity. A variety of paraviral syndromes associated with HIV infection such as QT prolongation, cachexia, cardiomyopathy, and lipodystrophy are consistent with evidence of autonomic dysfunction. Immunomodulatory effects of autonomic dysfunction toward Th2 bias are presented. A plausible mechanism by which HIV can influence autonomic balance through hypothalamic manipulation is offered. Shift to Th2 dominance is associated with HIV disease progression and can be viewed as a viral adaptation to promote its own survival. Autonomic remodeling by HIV may exemplify this phenomenon. Our hypothesis has implications for treatment of HIV and its associated syndromes.

Autonomic Nervous System Diseases↗

Autonomic function in cirrhosis assessed by cardiovascular reflex tests and 24-hour heart rate variability.

OBJECTIVES: To assess the prevalence of autonomic dysfunction in cirrhosis and to observe the effect of disease severity on autonomic dysfunction. METHODS: Seventy patients with cirrhosis (Child's class A, 42; Child's class B, 10; and Child's class C, 15) (45 alcoholic, 15 primary biliary cirrhosis, five chronic active hepatitis, and eight idiopathic) underwent standard cardiovascular reflex tests. In addition, in 40 patients, 24-h ECG RR variability tests were performed to detect autonomic dysfunction. RESULTS: Forty-two of 70 (60%) patients had abnormalities of cardiovascular reflex function of varying severity, whereas 24 of 34 (70%) had 24-h RR counts with the 95% age-related tolerance. The prevalence of abnormality increased with increasing severity of liver disease but not with different etiologies. CONCLUSION: Irrespective of etiology, there is a high prevalence of autonomic dysfunction in cirrhosis, and it is related to disease severity: the mechanism is unknown.

Autonomic Nervous System Diseases↗

Cardiac and autonomic evaluation in a pediatric population with human immunodeficiency virus.

BACKGROUND: Cardiac involvement in children with human immunodeficiency virus (HIV) infection is a well-known entity and occurs clinically more often in patients with advanced acquired immunodeficiency syndrome (AIDS). Autonomic dysfunction is less known, especially in children. HYPOTHESIS: The aim of this study was to asses the prevalence of cardiovascular abnormalities in a pediatric population with HIV. We also aimed to evaluate whether autonomic involvement occurs in the same population and is dependent on echocardiographic abnormalities. METHODS: The occurrence of echocardiographic abnormalities was evaluated in 22 children with HIV infection, and five noninvasive tests were performed to evaluate the presence of autonomic dysfunction. RESULTS: We found cardiac lesions in four children (18%), consisting of pericardial effusion in three children, wall motion abnormalities in three children, and acute aortic endocarditis in one child. All cardiac abnormalities were found at Stage C by Center for Disease Control (CDC) revised classification. We also found left ventricular filling pattern abnormalities consisting of E-wave maximal velocity decrease and prolonged deceleration time compatible with diastolic dysfunction. One of the five autonomic tests (Valsalva maneuver) was significantly altered, even in patients without abnormal echocardiography, suggesting mild autonomic dysfunction. CONCLUSION: The study demonstrated a high prevalence of cardiac lesions in children with HIV infection and indicated the presence of autonomic dysfunction even when there are no echocardiographically detected abnormalities.

Adolescent↗

Detection of silent myocardial ischemia in diabetes mellitus.

The prevalence of silent myocardial ischemia and its relation to autonomic dysfunction and pain threshold was studied in 58 men with diabetes mellitus and without cardiac symptoms. All patients underwent 48-hour ambulatory electrocardiographic monitoring and exercise testing after assessment of their autonomic function and pain threshold. Silent myocardial ischemia, defined as greater than or equal to 1 mm of ST-segment depression on either exercise testing or ambulatory electrocardiographic monitoring, was corroborated by exercise-induced reversible defect(s) on tomographic thallium scintigraphy. Autonomic function was assessed by heart rate response to: (1) Valsalva maneuver, (2) deep breathing, and (3) upright posture, as well as by diastolic blood pressure response to sustained handgrip and systolic blood pressure response to upright posture. Autonomic dysfunction was defined as greater than or equal to 2 abnormal responses. Pain threshold measurements were performed using electrical cutaneous stimulation of both forearms. Of the 58 diabetic patients, 21 were found to have autonomic dysfunction (36%). Silent myocardial ischemia was detected in 10 patients (17%), and was significantly more frequent in patients with than without autonomic dysfunction (38 vs 5%, p = 0.003). There was no difference in the electrical pain threshold or tolerance in subjects with and without silent myocardial ischemia. It is concluded that silent myocardial ischemia in asymptomatic diabetic men occurs frequently and in association with autonomic dysfunction, suggesting that diabetic neuropathy may be implicated in the mechanism of silent myocardial ischemia.

Adult↗

Clinical features of malignant syndrome in Parkinson's disease and related neurological disorders.

INTRODUCTION: We elucidated the cause and clinical characteristics of malignant syndrome (MS) in patients with Parkinson's disease (PD), early-onset parkinsonism (EOP), and other neurological disorders. MATERIALS AND METHODS: Subjects were 260 patients with PD or EOP, and three patients with other neurological disorders associated with MS. We studied clinical symptoms before and after the onset of MS, and evaluated autonomic function particularly before the onset of MS. RESULTS: The overall incidence of MS accompanying PD and EOP in our department was eight of 260 patients (3.1%). The incidence of MS in EOP was significantly higher than that in PD. All patients with MS showed comparatively longer duration of illness and advanced stage of PD and EOP. Factors triggering MS included reduced dosage or discontinuation of anti-parkinsonian drugs, reduction of oral intake, dehydration, infectious disease, postoperative state, and treatment with major tranquilizers. Although patients demonstrated marked autonomic symptoms at the onset of MS, in many cases autonomic dysfunction developed before the onset of MS. Even EOP patients, who usually demonstrated milder autonomic dysfunction, showed abnormalities in the correlation between circadian rhythm of blood pressure and pulse rate, and/or abnormal gastric emptying test, suggesting that autonomic dysfunction plays an important role in the cause of MS. Cooling the body, fluid replacement, resumption or increasing the dosage of anti-parkinsonian drugs and administration of dantrolene sodium overcame MS in all cases. CONCLUSION: Autonomic dysfunction is related to the cause and clinical features of MS in PD, EOP and some other neurological disorders.

Adult↗

Prolonged QT interval in alcoholic autonomic nervous dysfunction.

QT prolongation on electrocardiography is related to sudden cardiac death and is frequently found in alcoholics. We studied QT prolongation in relation to the function of cardiac autonomic nerves assessed by the coefficient of variation of the R-R interval (CVRR) in three age-matched groups of men: 32 alcoholics with autonomic nervous dysfunction (AN), 32 alcoholics without AN, and 32 healthy controls. The QTc interval and CVRR were measured at rest on the 30th day of abstinence, when electrolyte imbalance had disappeared. Subjects with arrhythmia, conduction abnormality, cardiomegaly, ischemic heart disease or diabetes mellitus were excluded. A CVRR of less than 80% of standard predicted value was judged to represent AN. In alcoholics, QTc correlated negatively with the ratio of CVRR to its standard value (r = -0.49, p < 0.0001). The incidence of QTc prolongation was higher in alcoholics with AN (46.9%) than in alcoholics without AN (21.9%, p < 0.05). QTc prolongation was not observed in healthy controls. The QTc interval was significantly (p < 0.01) longer in alcoholics with AN (444 +/- 20 msec) than in alcoholics without AN (426 +/- 17) and in healthy controls (398 +/- 18). These results suggest that alcoholism causes dysfunction of the autonomic nerves as well as worsening QT prolongation, and this may predispose such patients to sudden cardiac death.

Adult↗

Abnormalities of rate-corrected QT intervals in Parkinson's disease-a comparison with multiple system atrophy and progressive supranuclear palsy.

A number of patients with Parkinson's disease (PD) and multiple system atrophy (MSA), in whom sudden death does occur occasionally, have QT or rate-corrected QT (QTc) interval prolongation on electrocardiogram (ECG). Although these QT or QTc interval abnormalities are likely related to autonomic dysfunction, the pathophysiology remains unknown. The aim of this study was to compare the degree of QTc interval prolongation among akinetic-rigid syndromes, namely PD and related disorders, and to evaluate the relationship between QTc prolongation and severity of autonomic dysfunction. Thirty-four patients with PD, 22 with MSA, 11 with progressive supranuclear palsy (PSP) and 30 healthy controls underwent standard autonomic function tests, and electrocardiography variables (RR, QT and QTc intervals) were measured by an ECG recorder with an automated analyzer. The relationship between QTc interval and cardiovascular reflex tests were also analyzed. Orthostatic hypotension and decreased heart rate in response to respiratory stimuli were prominent in MSA, while these were relatively mild in PD. Unlike the RR and QT intervals, the QTc interval significantly differed among all groups (p<0.01). The QTc interval was significantly prolonged in PD (409+/-17 ms; p<0.001) and MSA (404+/-14 ms; p<0.05) compared with healthy controls (394+/-19 ms). Neither autonomic dysfunction nor QTc interval prolongation was evident in PSP. QTc intervals and cardiovascular reflexes did not correlate, except for Valsalva ratio. The QTc interval was obviously prolonged in PD patients to an extent that could not be accounted for simply by autonomic dysfunction levels. MSA patients showed slightly prolonged QTc intervals in spite of marked cardiovascular autonomic dysfunction. Abnormalities of the QTc may reflect the degeneration of cardioselective sympathetic and parasympathetic neurons that cannot be fully captured by cardiovascular autonomic function tests.

Adult↗

Autonomic related vertigo.

OBJECTIVES: To demonstrate clinical evidence that vestibular symptomatology can occur in relation to autonomic dysfunction. Characterization of clinical findings and treatment response would then allow autonomic related vertigo to be differentiated from other vertiginous conditions that present in a like manner. STUDY DESIGN: This was a retrospective review of 113 patients that described symptoms consistent with spontaneous, rotational vertigo and autonomic dysfunction. METHODS: Vestibular, otologic, and autonomic symptoms are presented along with the results of audiologic, orthostatic, and autonomic testing. Medical management included fluid loading, dietary changes, exercise, and patient education. Treatment results were analyzed according to the effectiveness in control of vestibular and otologic symptoms. Results were compared with a control group that demonstrated a similar vestibular and otologic presentation without autonomic symptomatology. RESULTS: All patients described spontaneous, rotational vertigo, with complete or substantial vertigo control obtained in 93 (85%) of 110 patients. Postural vertigo and distinct lightheadedness were also documented in 53% and 97% of cases, respectively. Vertigo failed to improve or worsened with prior treatment of low sodium diet or diuretic in 53 (91%) of 58 cases. Vertigo improvement was subsequently achieved in 48 (86%) of 56 cases with an autonomic treatment regimen. Long-term vertigo control was obtained in 56 (88%) of 64 patients followed for at least 18 months. Tinnitus was reported in 97 (86%) patients, aural fullness in 93 (82%) patients, and subjective hearing loss (HL) in 46 (41%) of 111 cases. Bilateral tinnitus and aural fullness occurred in 65% and 63%, respectively. Tinnitus improved with treatment in 56 (67%) of 84 patients, whereas aural fullness improved in 59 (74%) of 80 patients. Autonomic symptoms included palpitations in 103 (91%) patients, chronic fatigue in 102 (90%) patients, cold extremities in 91 (81%) patients, and previous fainting in 72 (64%) patients. A history of mitral valve prolapse was documented in 51 (45%) of cases and demonstrated with echocardiogram in 68 (93%) of the 73 patients tested. Audiologic testing was normal in 104 (95%) of 109 patients, and electrocochleography was abnormal in 42 (40%) of 105 patients. Orthostatic blood pressure and heart rate testing met the criteria for orthostatic hypotension in 16 (15%) of 104 patients. Autonomic testing was obtained in 34 cases, with orthostatic intolerance demonstrated in 33 (97%) patients and orthostatic hypotension demonstrated in 13 (38%) patients. Overall, orthostatic hypotension was documented through combined testing results in 23 (21%) of 107 patients. Vertigo was reproduced during autonomic testing in 17 (77%) of 22 patients, and otologic symptoms were reproduce in 9 (47%) of 19 patients. Comparison of the study population with a control group without autonomic symptoms revealed statistically significant differences in orthostatic testing and treatment results. There was no statistical difference noted in findings between patients of this study that demonstrated or failed to demonstrate orthostatic hypotension. CONCLUSIONS: There is a subgroup of patients with spontaneous vertigo who also demonstrate symptoms and findings consistent with poor autonomic regulation. These patients report vertigo improvement with a treatment strategy that aims to improve autonomic dysfunction through expansion of effective circulating volume. Clinical findings and treatment results of this study suggest an underlying autonomic influence in the production of vertigo and otologic symptoms.

Adolescent↗

Effect of posture on blood and intraocular pressures in multiple system atrophy, pure autonomic failure, and baroreflex failure.

BACKGROUND: Intraocular pressure (IOP) may be partially under systemic vascular control. This study examined whether a correlation exists between blood and intraocular pressures in patients with autonomic dysfunction. METHODS AND RESULTS: Eleven patients with 3 types of confirmed autonomic dysfunction (multiple system atrophy, pure autonomic failure, and baroreflex failure) were compared with age- and gender-matched controls and had IOP, systolic blood pressure, diastolic blood pressure, heart rates, and calculated mean arterial pressures (MAP) and mean ocular perfusion pressures (MOPP) measured in the supine, sitting, and standing positions. Data were analyzed with a general linear model repeated-measures ANOVA. All pressures for patients showed a dramatic decline (P<0.001) from supine to standing (MAP -31+/-14 mm Hg; IOP -6+/-3 mm Hg; MOPP -25+/-14 mm Hg) compared with controls (MAP +4+/-7 mm Hg; IOP -1+/-2 mm Hg; MOPP +6+/-7 mm Hg). There was no significant change in heart rate from supine to standing for patients compared with controls (P=0.648). Within both the multiple system atrophy (n=5) and pure autonomic failure (n=4) groups, all initial pressures were similar to control pressures in the supine position, whereas patients with baroreflex failure (n=2) had higher mean pressures than respective controls in the supine position. CONCLUSIONS: In autonomic dysfunction, a large decrease in MAP correlated with a large decrease in IOP. These data suggest that the autonomic nervous system, perhaps through an influence on systemic blood pressure, has a significant role in IOP regulation.

Adult↗

Sleep apnea and autonomic cerebrovascular dysfunction.

Changes in common carotid blood flow (CCF) and resistance index (RI), calculated from velocity waveforms by a noninvasive pulsed Doppler technique, were measured during apneic episodes and voluntary breath holding in five sleep apnea patients (SA) and during breath holding in five normal subjects (N). During apneic episodes averaging 27 s, CCF was reduced by 9% and RI increased by 4%, both trends being related to apneic duration. Internal carotid artery measurements in one SA indicated more dramatic changes in blood flow and RI than noted in CCF. During breath holding, CCF decreased significantly in SA but not in N, and RI showed a smaller reduction in SA. These changes in CCF and RI during sleep apnea are similar to those noted in anesthetized dogs where vasomotor waves and associated apneas were induced by elevating intracranial pressure. Previously reported recordings of ventilatory and systemic cardiovascular responses in SA are similar to these recordings in dogs, and it is therefore proposed that vasomotor responses to intermittent cerebral ischemia and hypercapnia may be the principle event in SA and periodic breathing only a secondary consequence of the prevailing autonomic dysfunction.

Animals↗

Relations among autonomic nerve dysfunction, oesophageal motility, and gastric emptying in gastro-oesophageal reflux disease.

Recent studies suggest that vagal nerve dysfunction may be important in the aetiology of gastro-oesophageal reflux disease. Delayed oesophageal transit and slowed gastric emptying occur frequently and may also be of pathogenic importance. In 48 patients with gastro-oesophageal reflux disease we studied the prevalence of and relations between autonomic nerve dysfunction (as assessed by cardiovascular reflex tests) and oesophageal transit, oesophageal motility, gastric emptying, and endoscopic grade of oesophagitis. Of the 48 patients, 21 (44%) had abnormal autonomic nerve function, which was predominantly parasympathetic. Oesophageal transit was delayed in 28% of the patients and gastric emptying of the solid component of the meal was delayed in 46%. Oesophageal transit was significantly (p less than 0.007) slower in patients with abnormal autonomic nerve function. The percentage of synchronous oesophageal contractions was related to the score for autonomic nerve dysfunction (r = 0.40, p less than 0.05). There was no significant relation of autonomic nerve dysfunction to either delayed gastric emptying or endoscopic grade of oesophagitis. We conclude that in gastro-oesophageal reflux disease there is a high prevalence of parasympathetic nerve dysfunction which relates to delayed oesophageal transit and abnormal peristalsis and may therefore be of pathogenic importance.

Adult↗

Effect of the somatostatin analogue SMS-201-995 on the adrenergic response to glucose ingestion in patients with postprandial hypotension.

PURPOSE: The somatostatin analogue SMS-201-995 has recently been introduced as a new therapy for postprandial hypotension in patients with autonomic neuropathy. The present study was performed to determine the effect of SMS-201-995 on the adrenergic response to glucose ingestion in patients with this disorder. PATIENTS AND METHODS: Eleven patients with postprandial hypotension were studied: six with central autonomic dysfunction (multiple system atrophy) and five with peripheral sympathetic dysfunction (progressive autonomic failure). Patients received either a subcutaneous injection of SMS-201-995 or a placebo injection, immediately before administration of a 50-g glucose drink. Each treatment was given on separate, consecutive days in a randomized fashion. RESULTS: Glucose ingestion caused a decrease in blood pressure (from 82 +/- 6 mm Hg to 66 +/- 7 mm Hg, p less than 0.01) and an increase in plasma norepinephrine level (165 +/- 20 pg/mL to 305 +/- 85 pg/mL, p less than 0.01) in five patients with progressive autonomic failure. Administration of SMS-201-995 prevented both the decline in blood pressure and the increase in norepinephrine. By contrast, glucose ingestion elicited no increase in plasma norepinephrine levels despite profound hypotension (average postprandial mean blood pressure, 55 +/- 3 mm Hg) in six patients with multiple system atrophy. Administration of SMS-201-995 prevented postprandial hypotension in these patients, but had no effect on plasma norepinephrine. CONCLUSION: Our data indicate that the pressor effect of SMS-201-995 is independent of the sympathetic nervous system in patients with multiple system atrophy, but may suppress the adrenergic response to glucose ingestion in patients with progressive autonomic failure.

Autonomic Nervous System Diseases↗

Autonomic dysreflexia and primary afferent sprouting after clip-compression injury of the rat spinal cord.

Spinal cord injury leads to many forms of autonomic dysfunction including autonomic dysreflexia, a condition involving recurrent episodes of paroxysmal hypertension and associated bradycardia. This hypertension may reach intensities that are life-threatening. We investigated autonomic dysreflexia and the sprouting of central processes of primary afferent neurons (a potential mechanism for autonomic dysreflexia) in a clinically-relevant calibrated clip-compression model of spinal cord injury in the rat. Autonomic dysreflexia was induced by colon distension in the conscious rats 2 weeks after severe (50-g) clip compression injury of the spinal cord at the 4th thoracic segment. The central arbor of small-diameter primary afferent fibers in laminae III-VII of the spinal cord dorsal horn was also assessed at 2 weeks after cord injury by quantitative morphometry, using calcitonin gene-related peptide as a marker. In response to colon distension, arterial pressure increased by 41 +/- 3 mmHg from a resting value of 109 +/- 4 mmHg, and heart rate decreased by 124 +/- 13 beats/min from a value of 515 +/- 16 beats/min (n = 7). Minimal locomotor function was recovered by these rats: by 2 weeks after injury they attained scores of only 3.1 +/- 1.3 on the Basso, Beattie and Bresnahan scale. Histopathology of the clip-compression lesion site in the cord consisted of extensive central necrosis extending several segments rostral and caudal to the lesion. Quantitative measures of the small-diameter afferent arbors revealed significant increases in area ranging from 20-27% in thoracolumbar segments caudal to the injury (n = 5) in comparison to sham-injured rats (n = 6). A second study was done to assess the impact of severity of injury on the relationship between the size of the primary afferent arbors and autonomic dysreflexia. At 2 weeks after milder (20-g) clip injury at T4, rats exhibited responses to colon distension that were not those associated with autonomic dysreflexia (n = 5). Arterial pressure increased by only 16 +/- 3 mmHg and heart rate tended to increase (+19 +/- 12 beats/min). These rats attained a locomotor score of 7.1 +/- 0.4 by 2 weeks. The lesions at the injury site also contained necrosis and mild cavitation within the gray matter. No change in the small-diameter afferent arbor was detected at 2 weeks after the 20-g clip injury at T4 (n = 6 rats). These findings suggest that after severe but not mild clip compression injury of the spinal cord, sprouting of the afferent component of the spinal reflex are contributes to the development of autonomic dysreflexia. Neither dysreflexia, nor changes in the afferent arbor size occurred after mild cord injury. This clinically relevant clip compression cord injury model, studied more frequently for locomotor function, is excellent for investigating mechanisms for the development of autonomic dysreflexia and strategies for its prevention.

Animals↗

The treatment of chronic extremity pain in failed lumbar surgery. The role of lumbar sympathectomy.

Persistent lower extremity pain after unsuccessful lumbar surgery continues to be a disabling condition. The results of deafferentation procedures for radiculopathy have been disappointing. Hence, the prospect of isolating a potentially reversible component of extremity pain is quite attractive. Given the frequency with which vasomotor complaints occur in this setting, the occurrence of autonomic dysfunction seems quite plausible. Autonomic dysfunction was investigated in 17 patients who had undergone previous lumbar surgery and had chronic limb pain. Patients underwent a preblockade thermogram, sympathetic blockade, and postblockade thermograms. All patients reported substantial relief after blockade, and all underwent retroperitoneal sympathectomy. All patients were followed for at least 2 years. The clinical results were disappointing, with only one patient reporting substantial relief. Although the results of thermography initially seemed to correlate with clinical outcome, further follow-up failed to yield any correlation. Additionally, no specific combination of response to blockade or thermogram was predictive of the clinical success after sympathectomy. Now, lumbar sympathectomy is not recommended in the setting of chronic radiculopathy and persistent extremity pain.

Female↗