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At least 325 records · Page 18Linked to original sources
PubMed1993

Autonomic dysfunction in patients with chronic intestinal pseudo-obstruction.

We prospectively evaluated autonomic function in 50 patients with clinical and manometric features of a neuropathic form of chronic intestinal pseudo-obstruction (CIP). In 26 patients, there were underlying disease processes that may have affected extrinsic neural control to viscera: diabetes mellitus (n = 16), previous gastric surgery (n = 5), and other neurologic disorders (n = 5). Our aim was to characterize autonomic function in these patients, and those 24 with CIP unassociated with a known underlying neurologic disorder (idiopathic group). We assessed vagal function and sympathetic cholinergic and adrenergic function by means of standardized autonomic tests and quantitated postprandial antral pressure activity. We also measured postprandial levels of pancreatic polypeptide and neurotensin as indicators of vagal function and of the delivery of nutrients to the distal small bowel. Among the idiopathic group (n = 24), two had evidence of a generalized sympathetic neuropathy and five abdominal vagal dysfunction (one had both). Among diabetic patients, three had sympathetic adrenergic failure, six had orthostasis with normal plasma noradrenaline, ten had signs of generalized sympathetic neuropathy and eight had abdominal vagal dysfunction. Vagal dysfunction was identified in all three patients who underwent vagotomy as part of their previous gastric surgery. In the other neurologic syndromes, vagal function was abnormal in three of the five patients. Thus, autonomic and, particularly, vagal dysfunction are confirmed in a majority of patients with CIP associated with known diabetes or neurologic disorders; however, a previously unrecognized autonomic (chiefly vagal) neuropathy of undetermined cause has been identified in five of the 24 'idiopathic' CIP patients.

Autonomic Nervous System Diseases↗
PubMed2002

Hypertension in orthostatic hypotension and autonomic dysfunction.

Disabling orthostatic hypotension dominates the clinical picture of autonomic failure. Nonetheless, severe supine hypertension is observed in about 50% of patients. In patients with multiple system atrophy (Shy-Drager syndrome), supine hypertension is explained by residual sympathetic tone because it can be eliminated with the ganglionic blocker trimethaphan. The cause of hypertension in patients with pure autonomic failure is not known and its understanding may be relevant to essential hypertension. Supine hypertension complicates the treatment of these patients but can be managed by overnight administration of antihypertensive medications.

Humans↗
PubMed1989

Cardiac autonomic dysfunction in obese subjects.

1. The prevalence of cardiac autonomic alterations was evaluated in 23 obese subjects with body mass index 37.2 +/- 3.03 kg/m2 (mean +/- SD), compared with 78 controls with body mass index 22.5 +/- 2.6 kg/m2 (P less than 0.001). 2. Cardiac autonomic function was assessed by four standard tests (heart rate response to deep breathing and to the Valsalva manoeuvre, systolic blood pressure fall after standing and diastolic pressure rise during handgrip) and by the cross-correlation test, a new method of computerized analysis of respiratory sinus arrhythmia based on spectral analysis of electrocardiographic and respiratory signal. 3. Considering tests indicative of parasympathetic function, only the heart rate response to the deep breathing and the cross-correlation test were significantly lower in the obese than in the control group [deep breathing = 13.95 +/- 8.65 beats/min (mean +/- SD) vs 24.5 +/- 7.65, P less than 0.001; cross-correlation 4.28 +/- 0.74 units vs 5.14 +/- 0.63, P less than 0.001]. Deep breathing and/or cross-correlation were abnormal in 10 (43.5%) obese subjects (deep breathing: seven subjects, cross-correlation: eight subjects). No significant difference between groups was found for the response to the Valsalva manoeuvre: the Valsalva ratio was 1.69 +/- 0.45 in obese subjects and 1.88 +/- 0.33 in controls (P = NS). The Valsalva ratio was abnormal in three obese subjects. 4. No significant differences were found between groups for tests indicative of sympathetic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Relationship between autonomic dysfunction and BP variability in subjects with diabetes mellitus.

Autonomic vagal heart rate (HR) control, office BP and ambulatory BP were examined in 54 diabetic subjects, aged 63 +/- 6 years. Sixteen subjects were insulin-dependent. The HR response to deep breathing (the bradypnoea test) was used to evaluate the vagal HR control, and ambulatory BP was determined by the Spacelabs 5200 system (one determination every 15 minutes, for 24 hours). Twenty-seven subjects had normal office BP (SBP < or = 140 mmHg and DBP < or = 90 mmHg), seven had established hypertension (SBP > or = 160 mmHg and DBP > or = 95 mmHg) and 30 were borderline hypertensives. Over the total group, office systolic/diastolic BP (mean +/- SD) was 142 +/- 20/85 +/- 10 mmg. Systolic/diastolic ambulatory BP was 123 +/- 13/77 +/- 10 mmHg and ambulatory HR was 70 +/- 8 beats/min. Because of the small age range of our subjects, the HR score was not correlated with age (r = 0.19, NS). The HR score was not correlated with the levels of office and ambulatory pressures. In contrast, it was significantly correlated with the variability of ambulatory SBP, whether the variability was defined by the pressure standard deviation, or by the ratio SD/mean value (r = 0.40, P = 0.005 and r = 0.33, P < 0.017, respectively). We suggest that an impairment of the autonomic control in diabetics might induce an increase in variability of SBP. BP variability might play a role in the cardiovascular complications observed in diabetics.

Aged↗
PubMed2004

[Psychosomatic ratios and their correction in the autonomic dysfunction of the sinus node].

The study was undertaken to examine the ratio of mental to somatic disorders in patients with autonomic sinus nodal dysfunction (ASND) and the capacities of correction of revealed disorders with the atypical benzodiazepine drug clonazepam. Thirty-two patients with ASND were examined. The diagnosis of ASND was verified by 24-hour ECG monitoring and transesophageal atrial pacing, by performing autonomic cardiac block with atropine and obsidan. In addition to physical examination, heart rhythm variability was studied during relaxed and intensive wake; psychological studies using the conventional tests were conducted, and autonomic disorders were explored by means of original scored somatic, hyperventilation) questionnaires. After examination, the patients received a 1.5-to-2-month course of therapy with clonazepam in a daily dose of 1.5-2 mg. The study has revealed that clinical symptomatology in ASND is greatly determined by psychosomatic disorders. ASND was marked by anxious depressions in combination with inadequate peripheral (to a greater extent, sympathetic) neurovegetative exposures with the simultaneous activation of cerebral ergotropic effects. The use of clonazepam in ASND greatly improved its clinical picture, by eliminating, in the overwhelming majority of cases, clinical symptoms, including rhythm and conduction disturbances that are characteristic of ASND.

Adult↗
PubMed1990

The relationship between locomotor disability, autonomic dysfunction, and the integrity of the striatal dopaminergic system in patients with multiple system atrophy, pure autonomic failure, and Parkinson's disease, studied with PET.

18F-dopa and S-11C-nomifensine (NMF) are positron emitting tracers whose caudate and putamen uptake reflects striatal dopamine storage capacity and the integrity of dopamine reuptake sites, respectively. Using these two tracers, the integrity of the presynaptic striatal dopaminergic system has been studied with positron emission tomography (PET) in 10 subjects with multiple system atrophy (MSA, Shy-Drager syndrome) who had an akinetic-rigid syndrome that was poorly responsive to L-dopa, autonomic failure, and cerebellar ataxia. PET findings for the 10 MSA patients were compared with those for 13 age-matched controls, 8 subjects with L-dopa responsive Parkinson's disease (PD), and 7 subjects with pure autonomic failure (PAF). Influx constants, Ki, reflecting specific 18F-dopa uptake into striatal tissue, were severely reduced in the putamen and caudate of the 10 MSA subjects (mean putamen Ki 0.005 min-1 MSA vs 0.013 min-1 controls; mean caudate Ki 0.007 min-1 MSA vs 0.013 min-1 controls). Reduction of putamen, but not caudate, 18F-dopa uptake correlated with severity and duration of locomotor disability. Eight patients with PD, and a similar degree and duration of locomotor disability to the patients with MSA, demonstrated equal impairment of mean putamen 18F-dopa uptake, but significant preservation of mean caudate function. The 7 PAF patients had normal mean levels of putamen and caudate 18F-dopa uptake, although 1 individual PAF patient had significantly impaired striatal function. The MSA and PD groups of subjects both showed significantly reduced levels of specific striatal S-11C-NMF binding, again caudate function being relatively preserved in PD. It is concluded that in both MSA and PD there is a parallel decline of striatal dopamine storage capacity and reuptake site integrity, probably reflecting a loss of nigrostriatal nerve terminals. Caudate function is relatively preserved in PD compared with MSA. The majority of PAF patients have an intact nigrostriatal dopaminergic system, suggesting that PAF is a condition distinct from PD and MSA in spite of some pathological similarities. PET is capable of detecting subclinical nigrostriatal involvement in PAF patients when this is present.

Adult↗
PubMed1988

Autonomic dysfunction in recent onset and advanced Parkinson's disease.

Cardiovascular autonomic nerve function and its relation to the clinical variables of untreated recent onset and levodopa-treated advanced disease parkinsonian patients were studied. Heart rate variations were diminished in both groups when compared with age-matched controls. An orthostatic blood pressure drop was found in both disease groups. The drop was stronger and related to the levodopa dose in the advanced disease group. In conclusion, 1) in Parkinson's disease a parasympathetic damage occurs which worsens during the course of the disease, 2) the orthostatic fall in blood pressure, indicating a sympathetic dysfunction, is partly due to the disease itself and partly due to levodopa treatment.

Aged↗
PubMed2006

Autonomic dysfunction in spinal cord injury: clinical presentation of symptoms and signs.

Spinal cord injury and especially cervical spinal cord injury implies serious disturbances in autonomic nervous system function. The clinical effects of these disturbances are striking. In the acute phase, the autonomic imbalance and its effect on cardiovascular, respiratory system and temperature regulation may be life threatening. Serious complications such as over-hydration with the risk of pulmonary edema or hyponatremia are seen. The cord-injured person suffers from autonomic nervous system dysfunction also affecting bladder and bowel control, renal and sexual function. Paralytic ileus may cause vomiting and aspiration, which in turn interferes with respiratory function in those with cervical spinal cord injury. The cord-injured person is at risk to develop pressure sores from the moment of the accident. Two to three months post-injury the cord-injured person with a lesion level above the fifth thoracic segment may develop autonomic dysreflexia, characterised by sympathetically mediated vasoconstriction in muscular, skin, renal and presumably gastrointestinal vascular beds induced by an afferent peripheral stimulation below lesion level. The reaction might cause cerebrovascular complications and has effects on metabolism. Some of the autonomic disturbances are transient and a new balance is reached months post-injury, while others persist for life.

Autonomic Dysreflexia↗
PubMed1998

Autonomic dysfunction in patients with achalasia of the oesophagus.

It has been suggested that achalasia is associated with extraoesophageal sympathetic and parasympathetic dysfunction. In a prospective study we applied conventional ultrasonography and duplex sonography to investigate basal and postprandial peak systolic velocity (PSV), pulsatility index (PI) and resistance index (RI) of superior mesenteric artery and PSV of portal vein in nine patients with achalasia and 10 healthy controls (study I). In addition, in eight of these patients autonomic nervous function was investigated by pupillary function tests as well as cardiovascular reflex tests and compared with eight age- and sex-matched controls (study II). The results indicated that postprandial increase of PSV in the superior mesenteric artery was significantly lower, and postprandial decrease of PI and RI significantly higher in achalasia compared to healthy controls. In contrast, postprandial increase of PSV in the portal vein was not significantly different between both groups. Autonomic function tests revealed significant lower maximal pupillary contraction and redilatation velocities, significantly lower heart rate variation during orthostasis, deep respiration test and Valsalva manoeuvre in achalasia compared to controls. It is concluded that achalasia is associated with extraoesophageal autonomic nervous dysfunction that involves cardiovascular and pupillary function as well as regulation of mesenteric arterial blood flow.

Adult↗
PubMed1995

Sleep-apnoea and autonomic dysfunction: a cardiopressor and pupillometric study.

Isolated alterations in the autonomic nervous system (ANS) have been described in obstructive sleep-apnea syndrome (OSAS), but the exact nature and degree of ANS involvement in OSAS is as yet uncharted. In the present study we evaluated some autonomic nervous functions in 13 OSAS patients using cardiopressor and pupillometric tests. Almost all showed only slight alterations of ANS function, generally in the form of a hypofunction of both sympathetic and parasympathetic branches. Pupillometry was more sensitive than cardiovascular indexes in detecting neurovegetative involvement which correlated with some respiratory indices. The data suggest that autonomic involvement in OSAS is ascribable to metabolic changes (hypoxia, hypercapnia) rather than to primary "neurogenic" alterations.

Adult↗