Surgical aspects of autonomic dysreflexia

Autonomic dysreflexia (AD) is a characteristic syndrome that occurs in spinal cord injury (SCI) patients with lesions above the sympathetic outflow at T6 and rarely in those with lesions below T10. Symptoms are initiated by noxious stimuli below the level of injury which result in massive sympathetic discharges from the isolated cord. These produce what may be called a sympathetic storm manifest by severe life threatening hypertension. Anesthesiologists and surgeons dealing with SCI patients must know how to recognize this syndrome, how to prevent its occurrence and how to manage it aggressively. Choice of anesthesia is frequently difficult and, in particular, it may be difficult to decide which type of anesthesia is best for patients susceptible to the syndrome. Therefore, we have conducted a retrospective study of SCI patients in the Department of Veterans Affairs Medical Center, Long Beach, California, where the Spinal Cord Injury Service is one of the largest in the country.     

Urethral closing pressure after spinal cord injury and its relationship to autonomic dysreflexia

The evolution of patterns of neurogenic vesical dysfunction with emphasis on urethral resistance has been studied using a two-catheter urethral profile technique in 24 patients following acute spinal cord injury. Inappropriate urethral resistance to voiding appeared to result both from smooth and skeletal muscular activity and to some extent was dependent on the level of the spinal cord lesion. Autonomic dysreflexia was common, and responded to treatment with an alpha-sympatholytic agent.     

Autonomic dysreflexia during urodynamics

Autonomic dysreflexia (AD) is an acute syndrome characterised by inappropriate and massive autonomic response that occurs in patients with spinal cord injury above the T6 level. AIMS: to evaluate the incidence of AD during cystometry and the relationships with clinical and urodynamic features. PATIENTS AND METHODS: Forty-eight spinal cord injury patients were studied by neurological and urological examination and urodynamic evaluation with concurrent recording of blood pressure, heart rate and symptoms and signs of AD. Patients were considered to have AD if blood pressure reached values higher than 150/100 mmHg. RESULTS: All the patients showed a significant increase of both systolic and diastolic blood pressure, although only 20 showed pressure values higher than 150/100 mmHg (in seven of them without AD symptoms). AD was more frequent in cervical patients (P = 0.034), but did not correlate with any other clinical features: sex ratio, age, disease duration, completeness of lesion, incidence of detrusor hyperreflexia/areflexia and detrusor-sphincter dyssynergia, voiding modalities, usage of anticholinergic drugs. In three patients blood pressure increase began when uninhibited contraction started, in 11 it was coincident with uninhibited contraction peak and in the other six it appeared at maximum bladder capacity. CONCLUSIONS: (1) during urodynamic evaluation all the patients with lesion level above T6 showed signs of sympathetic stimulation, although only some showed dangerous blood pressure values; (2) the relationship between urodynamic data and dysreflexia crisis shows that both the presence of detrusor uninhibited contractions and bladder distension are able to stimulate the crisis; (3) treatment with anticholinergic drugs is not sufficient to prevent autonomic dysreflexia starting from the bladder, unless it induces detrusor areflexia. These patients are at risk of developing autonomic dysreflexia following bladder distension.     

Changes in the morphology of sympathetic preganglionic neurons parallel the development of autonomic dysreflexia after spinal cord injury in rats

Following spinal cord transection (SCT), sensory input to the spinal cord causes increases in arterial pressure that are small in rats 1 week after SCT, but become large and well established by 2 weeks. Moreover, sympathetic preganglionic neurons (SPNs) undergo atrophy by 1 week after SCT, and regeneration of these neurons may be an important factor in the etiology of this autonomic dysreflexia. Therefore, we examined the morphology of SPNs 2 weeks after SCT using retrograde transport of the cholera toxin subunit B. The dendritic arbors of SPNs were re-established by 2 weeks after SCT. This regeneration parallels the time course of the development of autonomic dysreflexia after cord injury in the rat, and may play a role in initiating this disorder.     

The hypertension of autonomic failure and its treatment

We studied the incidence and severity of supine hypertension in 117 patients with severe primary autonomic failure presenting to a referral center over a 9-year period. Patients were uniformly characterized by disabling orthostatic hypotension, lack of compensatory heart rate increase, abnormal autonomic function tests, and unresponsive plasma norepinephrine. Fifty-four patients had isolated autonomic impairment (pure autonomic failure). Sixty-three patients had central nervous system involvement in addition to autonomic impairment (multiple-system atrophy). Patients were studied off medications, in a metabolic ward, and on a controlled diet containing 150 mEq of sodium. Fifty-six percent of patients had supine diastolic blood pressure > or =90 mm Hg. The prevalence of hypertension was slightly greater in females (63%) than in males (52%). Potential mechanisms responsible for this hypertension were investigated. No correlation was found between blood volume and blood pressure. Similarly, plasma norepinephrine (92+/-15 pg/mL) and plasma renin activity (0.3+/-0.05 ng/mL per hour) were very low in the subset of patients with pure autonomic failure and supine hypertension (mean systolic/diastolic pressure, 177 +/- 6/108 +/- 2 mm Hg, range 167/97 to 219/121). Supine hypertension represents a challenge in the treatment of orthostatic hypotension. We found these patients to be particularly responsive to the hypotensive effects of transdermal nitroglycerin. Doses ranging from 0.025 to 0.1 mg/h decreased systolic blood pressure by 36+/-7 mm Hg and may effectively treat supine hypertension overnight, but the dose should be individualized and used with caution.     

Serratus anterior dysfunction. Recognition and treatment

Recognition of scapular winging may be difficult, and potential errors in treatment can result. Such treatment errors may cause morbidity for the patient. In addition, electrical evidence of long thoracic nerve injury usually is required to confirm the etiology of scapular winging as being caused by serratus anterior dysfunction. Although various conditions may result in scapular winging, primary serratus anterior dysfunction can be treated effectively by transfer of the pectoralis major tendon; however, this surgical approach sometimes may given an unacceptable cosmesis, and there may be local morbidity to the donor site of the iliotibial band graft that is used to augment the tendon transfer. The authors report eight patients with primary chronic scapulothoracic winging refractory to conservative treatment. Five of these patients had an incorrect diagnosis, and this resulted in 17 surgical procedures without resolution of their pain or improvement of function. Of the eight patients who required additional surgery to stabilize the scapula, only five patients had an electromyographic study that showed long thoracic nerve palsy, although all patients had profound scapulothoracic winging. All patients underwent a modified pectoralis major transfer with autogenous semitendinosus and gracilis tendon augmentation using two small incisions. Although one patient had a postoperative infection develop, the remaining seven patients had resolution of their winging, improved function, and satisfactory cosmesis.     

Failure of erythropoietin treatment in a case with primary autonomic failure

All prisons provide healthcare services which aim to meet the needs of prisoners. The goal of the service is to give prisoners access to the same quality and range of health care as the NHS gives the general public. However, within the prison environment priorities centre around order, control and discipline and therefore an ethos of health care needs to be developed. Custody reduces the prisoner's opportunity for self-care and independent action as inmates have to consult nursing or medical staff for even the most simple remedies. Nursing staff in the prison service can play a significant part in primary health care, mental disorder and health promotion. Nurses have the knowledge, skills and attitudes needed to deal with this diverse and vulnerable prison population and to promote a positive interface between custody and care.     

Fear and autonomic arousal.

32 female undergraduates were classified as having high fear (HF) or low fear (LF) of spiders. After reduction of orienting responses to pictures of neutral animals, experimental Ss were shown pictures of a spider, and control Ss were shown pictures of a snake. Using the response to the last neutral stimulus as a base line, HF experimental Ss when 1st shown a spider yielded greater GSRs than other groups. This increase in GSR responding for HF experimental Ss was, for 2 more trials, maintained relative to control Ss. HF experimental Ss also yielded GSRs of greater duration than all other groups when 1st shown the spider stimulus. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Psychopathy and autonomic conditioning.

Utilized a delayed, differential paradigm to investigate electrodermal, cardiac, and vasomotor conditioning in 18 psychopathic, 18 nonpsychopathic, and 18 "mixed" inmates. 3 tones, each 10 sec. long, were presented 16 times each in random order, alone, or followed by a shock or slide of a nude female. The psychopaths gave very little evidence of differential electrodermal conditioning. However, they acquired differential cardiac and digital vasomotor responses just as readily as did the nonpsychopaths to the CS followed by shock or by slides. Neither group gave any evidence of differential cephalic vasomotor conditioning. The psychopaths exhibited a lower level of tonic electrodermal activity and were less electrodermally responsive than were the other Ss. There were no differences between groups in tonic heart rate or in cardiac or digital vasomotor responsivity. However, the psychopaths responded to shock with cephalic vasodilation while the nonpsychopaths responded with vasoconstriction. (34 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Composite autonomic scoring scale for laboratory quantification of generalized autonomic failure

An autonomic reflex screen, which consisted of a quantitative sudomotor axon reflex test, orthostatic blood pressure and heart rate response to tilt, heart rate response to deep breathing, the Valsalva ratio, and beat-to-beat blood pressure measurements during phases II and IV of the Valsalva maneuver, tilt, and deep breathing, was used to develop a 10-point composite autonomic scoring scale of autonomic function. The scheme allots 4 points for adrenergic and 3 points each for sudomotor and cardiovagal failure. Each score is normalized for the compounding effects of age and sex. Patients with a score of 3 or less on the composite autonomic scoring scale have only mild autonomic failure, those with scores of 7 to 10 have severe failure, and those with scores between these two ranges have moderate autonomic failure. The sensitivity and specificity of the method were assessed by evaluating the composite autonomic scoring scale in four groups of patients with known degrees of autonomic failure: 18 with multisystem atrophy, 20 with autonomic neuropathy, 20 with Parkinson's disease, and 20 with peripheral neuropathy but no autonomic symptoms. The composite scores (means +/- SD) for these four groups, respectively, were as follows: 8.5 +/- 1.3, 8.6 +/- 1.2, 1.5 +/- 1.1, and 1.7 +/- 1.3. Patients with symptomatic autonomic failure had scores of 5 or more, those without symptomatic autonomic failure had scores of 4 or less, and no overlap existed in these groups. Thus, autonomic laboratory tests should be useful in grading the degree of autonomic failure.     

Major depression and cardiac autonomic control

We investigated autonomic control of heart rate in patients with major depression, melancholic type. Twenty-three depressed inpatients who were being treated with tricyclic antidepressants and 23 depressed patients who were taking no medications were compared with age- and sex-matched control groups on resting cardiac vagal tone and heart rate. In unmedicated depressed patients, cardiac vagal tone was comparable to that of control subjects, but heart rate was significantly higher. This increase in heart rate may have been due to sympathetic activation caused by anxiety, since the depressed patients were significantly more anxious than the control subjects. Medicated patients exhibited diminished cardiac vagal tone and higher heart rate than unmedicated patients and controls. This was probably due to the anticholinergic effects of the antidepressants. Our findings suggest that cardiac vagal tone is not lower than normal in patients with depression, melancholic type.     

Operant autonomic conditioning and rod-and-frame test performance

Forty subjects were administered the portable rod-and-frame test (RFT) before and after operant autonomic conditioning training or control experiences. Ten subjects were assigned to each of four groups: a heart rate conditioning group; a false heart rate feedback group; a galvanic skin-response conditioning group; and a control group. Half of the subjects in the three experimental groups were informed of the response-reinforcement contingencies, and half were not informed. Informed subjects in the conditioning groups exhibited significantly lower portable RFT scores after conditioning. The results suggest that awareness of and control over autonomic functioning may be an important determinant of RFT performance.     

Airway autonomic nervous system dysfunction and asthma

Airways are richly innervated by 4 nervous systems: adrenergic, cholinergic, inhibitory nonadrenergic noncholinergic (i-NANC), and excitatory NANC (e-NANC) nervous systems. Dysfunction or hyperfunction of these systems may be involved in the inflammation or airway hyperresponsiveness observed in asthmatic patients. The cholinergic nervous system is the predominant neural bronchoconstrictor pathway in humans. Airway inflammation results in exaggerated acetylcholine release from cholinergic nerves via dysfunction of the autoreceptor, muscarinic M2, which is possibly caused by a major basic protein or IgE. Vasoactive intestinal peptide (VIP) and nitric oxide (NO) released from i-NANC nerves act as an airway smooth muscle dilator. The effects of VIP and NO are diminished after allergic reaction by inflammatory cell-mediated tryptase and reactive oxygen species. Thus, in asthmatic airways, the inflammatory change-mediated neural imbalance may result in airway hyperresponsiveness. Tachykinins derived from e-NANC nerves have a variety of actions including airway smooth muscle contraction, mucus secretion, vascular leakage, and neutrophil attachment; and they may be involved in the pathogenesis of asthma. Since tachykinin receptor antagonists are effective for bradykinin- and exercise-induced bronchoconstriction in asthmatic patients, these drugs may be useful for asthma therapy.