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PubMed2004

Effects of epilepsy on autonomic nervous system and respiratory function tests.

We have investigated autonomic nervous system function during the interictal period in epileptic patients and the possible effects of autonomic dysfunction on respiratory functions. A total of 32 epileptic patients (23 generalized, 9 partial epilepsy) and 32 healthy volunteers were involved. Sympathetic skin response (SSR), for evaluating the sympathetic nervous system, and RR interval variation (RRIV) were measured at the beginning and third month of antiepileptic treatment, and respiratory function tests (RFTs) were performed. In patients with partial epilepsy, SSR latency in the upper extremity (1.3+/-0.2 s) was longer than that of controls (1.2+/-0.3 s) at baseline (P=0.05), and was significantly reduced (1.1+/-0.3 s) after treatment (P<0.05). RRIV values of patients with generalized epilepsy were statistically significantly lower than those of controls (P<0.01). However, deep breathing RRIV values (32.6+/-15.3%) of patients were lower than those (43.0+/-18.2%) of controls (P<0.05). Sympathetic dysfunction was determined in patients with partial epilepsy and parasympathetic dysfunction in patients with generalized epilepsy. No abnormality was observed on RFTs for both patients with partial epilepsy and patients with generalized epilepsy.

Adolescent↗
PubMed2002

Progressive supranuclear palsy: neuronal and glial cytoskeletal pathology in the higher order processing autonomic nuclei of the lower brainstem.

The medial and lateral parabrachial nuclei (MPB, LPB), the gigantocellular reticular nucleus (GI), the raphes magnus (RMG) and raphes obscurus nuclei (ROB), as well as the intermediate reticular zone (IRZ) represent pivotal subordinate brainstem centres, all of which control autonomic functions. In this study, we investigated the occurrence and severity of the neuronal and glial cytoskeletal pathology in these six brainstem nuclei from 17 individuals with clinically diagnosed and neuropathologically confirmed progressive supranuclear palsy (PSP). The association between the severity of the pathology and the duration of the disease was investigated by means of correlation analysis. The brainstem nuclei in all of the PSP cases were affected by the neuronal cytoskeletal pathology, with the IRZ and GI regularly showing severe involvement, the MPB, RMG, and ROB marked involvement, and the LPB mild involvement. In the six nuclear greys studied, glial cells undergo alterations of their cytoskeleton on an irregular basis, whereby diseased oligodendrocytes predominantly presented as coiled bodies and affected astrocytes as thorn-shaped astrocytes. In all six nuclei, the severity of the neuronal or glial cytoskeletal pathology showed no correlation with the duration of PSP. In view of their functional role, the neuronal pathology in the nuclei studied offers a possible explanation for the autonomic dysfunctions that eventually develop in the course of PSP.

Aged↗
PubMed1987

Spectral analysis of fluctuations in heart rate: an objective evaluation of autonomic nervous control in chronic renal failure.

A quantitative, noninvasive method of assessing autonomic control, based on the spectral analysis of beat-to-beat fluctuations in heart rate (HR), was applied to patients with chronic renal failure (RF). Since the power spectrum of HR fluctuations measures the dynamic nervous control of HR, it can be used to quantitate a normal control system as opposed to a disturbed or depressed system. Indeed, in RF patients, a strong reduction in the HR power spectrum was observed in all frequency ranges, both sympathetically and parasympathetically mediated. A similar depression in autonomic control was demonstrated in patients on hemodialysis or peritoneal dialysis. RF patients not yet undergoing dialysis show a lesser degree of depression. Spectral analysis of HR fluctuations in RF patients makes it possible to quantitate autonomic dysfunction and to reliably measure its development as a function of time, and requires only a 10-min standard electrocardiogram recording.

Adult↗
PubMed1987

Cerebral blood flow and calcium antagonists in hypertension.

Antihypertensive treatment reduces the risk of ischaemic strokes and cerebral haemorrhage as complications of excessive or long-standing hypertension. However, neurological dysfunction and brain damage may also accompany acute and, under certain conditions, even chronic antihypertensive treatment. Treatment should therefore be instituted restrictively and cautiously, with special regard to the action of antihypertensive drugs on cerebral perfusion in patients with an increased risk for treatment-induced cerebral ischaemic complications, e.g. patients with hypertensive encephalopathy, patients with autonomic dysfunction or elderly patients with suspected sclerotic stenosis of cerebral or neck arteries. The present study is a review of the structural and functional lesions of cerebral vessels observed in acute and chronic hypertension, together with the effects of antihypertensive drugs on cerebral blood flow. Calcium channel blockers such as nifedipine, nitrendipine and verapamil may have advantages as first-line drugs in the treatment of patients with an elevated risk for cerebral hypoperfusion, because of their selective action on vasoconstricted vessels and their differential effects in different regional vascular beds. The particular efficacy of calcium antagonists in acute antihypertensive treatment, with a significant increase in cerebral blood flow in the case of nifedipine, and also in chronic antihypertensive therapy without decreasing cerebral blood flow, may change the traditional management of hypertensive emergencies, as well as of other patients at risk of treatment-induced complications.

Aged↗
PubMed1997

Distinction of idiopathic Parkinson's disease from multiple-system atrophy by stimulation of growth-hormone release with clonidine.

BACKGROUND: Idiopathic Parkinson's disease is a common neurodegenerative disease that is difficult to distinguish from other parkinsonian syndromes such as multiple-system atrophy (MSA). In MSA, autonomic dysfunction is common and is associated with either parkinsonian or cerebellar features, or both. Differentiation of idiopathic Parkinson's disease from MSA is important because prognosis, complications, and response to therapy vary according to disorder. Our aim was to find out whether clonidine/growth hormone (GH) testing distinguishes idiopathic Parkinson's disease from MSA. METHODS: Clonidine is a centrally active alpha 2-adrenoceptor agonist that raises concentrations of GH in serum in healthy people and those with pure autonomic failure (with peripheral lesions), but not in those with MSA (with a central autonomic deficit). We investigated the effects of clonidine on 14 people with idiopathic Parkinson's disease (without autonomic deficits). 31 people with MSA of the three different clinical forms (parkinsonian, cerebellar, and mixed), 19 people with pure autonomic failure, and 27 healthy participants. In nine people with parkinsonian MSA (MSA-P), the GH response to levodopa was also assessed. FINDINGS: Clonidine raised serum GH concentrations in patients with idiopathic Parkinson's disease (median increase 8.98 [IQR 6.6-16.6] mU/L), normal participants (13.2 [7.0-18.6] mU/L), and patients with pure autonomic failure (12.5 [5.6-18.2] mU/L). In those with MSA who had central autonomic failure, GH concentrations were unchanged (MSA-P; 0.41 [-0.30 to 2.09] mU/L and cerebellar MSA [MSA-C] 1.67 [0-4.49] mU/L). The GH response to clonidine in idiopathic Parkinson's disease was significantly different from that in MSA-P (p < 0.0002). In MSA-P, the dopamine precursor levodopa raised GH concentrations (from mean 2.7 [SE 1.0] mU/L to mean 18.2 [6.0] mU/L, p < 0.05) and GH-releasing hormone (GHRH) concentrations (from mean 20.6 [3.25] ng/L to mean 68.0 [10.6] ng/L, p < 0.05), excluding dysfunction of pituitary somatotrophs or GHRH neurons as a cause for the absent GH response to clonidine in MSA. INTERPRETATION: The GH responses to clonidine clearly differentiated idiopathic Parkinson's disease from MSA-C and MSA-P. Together with the levodopa studies they indicated a specific alpha 2-adrenoceptor-hypothalamic deficit in MSA. The clonidine-GH test may provide further insight into central neurotransmitter and alpha 2-adrenoceptor-hypothalamic abnormalities in MSA.

Adrenergic alpha-Agonists↗
PubMed2002

Small fibre neuropathy in sarcoidosis.

Some patients with sarcoidosis have unexplained pain and dysaesthesia. We did quantitative sensory testing in 31 sarcoidosis patients with pain or autonomic dysfunction. 25 patients had reduced warmth sensitivity, cold sensitivity, or both. Intraepidermal nerve fibre density (IENFD) was measured in punch biopsy skin samples in seven consecutive patients. All seven patients had reduced IENFD compared with controls, which confirmed the presence of small fibre neuropathy in these patients. Some patients with sarcoidosis may have small fibre neuropathy with autonomic involvement.

Adult↗
PubMed1997

Magnesium sulphate for control of spasms in severe tetanus. Can we avoid sedation and artificial ventilation?

A prospective pilot study was undertaken to investigate the ability of magnesium sulphate to control the spasms of severe tetanus without the need for sedation and artificial ventilation. All eight patients admitted with severe tetanus to our intensive care unit within the last year were given magnesium sulphate intravenously as a 5-g loading dose followed by an infusion of 2-3 gh-1. The infusion rate was increased to control spasms while retaining the patella tendon reflex, which proved a valid guide to avoid overdose. Spasms were effectively controlled and serum magnesium concentrations were maintained within the therapeutic range. Spontaneous ventilation was adequate, ventilatory support being required only for the management of lung pathology. There was no evidence of cardiovascular instability due to sympathetic over activity. No supplementary sedation was required for the control of spasms or autonomic dysfunction during magnesium therapy. We conclude that magnesium sulphate can be used as the sole agent for the control of spasms in tetanus without the need for sedation and artificial ventilation.

Adult↗
PubMed1992

Rationale for the need to employ a conservative method in the treatment of patients with dystrophy of the hand.

Radioimmunoassay determining sexual hormone levels, functional state of the autonomic nervous system and blood supply, were used to study the causes aiding the development of dystrophies of the hand in women. All these conditions were found to be associated with gross disorders of the endocrine system, autonomic dysfunction and changes in the system of blood supply. The results were used to develop a policy for the selection of the therapeutic method and its timing with a favourable effect.

Adult↗
PubMed1992

Autonomic involvement in systemic diseases.

It is now well recognized that autonomic dysfunction may occur in disorders affecting the various body systems. Over the past year important observations have been reported in congestive cardiac failure, reflex sympathetic dystrophy (RSD), acquired immune deficiency syndrome (AIDS) and diabetes mellitus.

Autonomic Nervous System↗
PubMed1990

Myocardial mechanics in young adult patients with diabetes mellitus: effects of altered load, inotropic state and dynamic exercise.

The disease entity "diabetic cardiomyopathy" has been extensively described in young patients with diabetes in the absence of ischemic, hypertensive or valvular heart disease. The most convincing data have been a 30% to 40% incidence of decreased radionuclide angiographic left ventricular ejection fraction response to dynamic exercise. In the current study, the hypothesis was tested that this abnormal ejection fraction response was due to alterations in ventricular loading conditions or cardiac autonomic innervation (extrinsic factors), or both, rather than to abnormalities in intrinsic ventricular systolic fiber function (contractility). Twenty normotensive patients with diabetes (mean age 30 +/- 5 years, mean duration 15 +/- 6 years) and 20 age-matched normal subjects were studied. All patients with diabetes had a normal treadmill exercise tolerance test without evidence of myocardial ischemia. By radionuclide angiography, all normal subjects increased ejection fraction with exercise (62 +/- 4% to 69 +/- 6%; p less than 0.001). In contrast, 11 (55%) of 20 patients with diabetes maintained or increased ejection fraction with exercise (group 1; 62 +/- 4% to 69 +/- 6%; p less than 0.001) and 9 (45%) of 20 showed an exercise-induced decrease (group 2; 73 +/- 4% to 66 +/- 6%; p less than 0.001). No difference in the incidence of microangiopathy, as noted by funduscopic examination, was present between the diabetic groups. Despite the abnormal ejection fraction response to exercise in the group 2 patients with diabetes, all patients with diabetes had a normal response to afterload manipulation, normal baseline ventricular contractility as assessed by load- and heart rate-independent end-systolic indexes and normal contractile reserve as assessed with dobutamine challenge. Autonomic dysfunction did not explain the disparate results between the group 2 patients' radionuclide angiographic data and their load-independent tests of ventricular contractility and reserve. In addition, the high ejection fraction at rest in group 2 patients (73 +/- 4% versus 62 +/- 4% for normal subjects; p less than 0.001) was not related to the abnormal tests of autonomic function. Thus, when left ventricular systolic performance was assessed by load- and rate-independent indexes, there was no evidence for cardiomyopathy in young adult patients with diabetes who have normal blood pressure and no ischemic heart disease.

Adult↗
PubMed1999

Twenty-four-hour heart rate variability to assess autonomic function in Parkinson's disease.

OBJECTIVES: To evaluate the autonomic dysfunction in Parkinson's disease patients by means of a 24-h heart rate variability (HRV) method. MATERIAL AND METHODS: Thirteen patients with a diagnosis of Parkinson's disease were compared with 13 age-matched healthy persons (control group). The 13 patients had a mean age of 70.5 years, and mean disease duration of 10.9 years. The autonomic function was evaluated by HRV analysis using a continuous 24-h ECG. The parameters of SDNN (standard deviation of the normal-to-normal intervals between adjacent QRS complexes), of LF (power in low frequency) and of HF (power in high frequency) were studied during the following 3 periods: 24 h, night and day. RESULTS: The data show a statistically significant difference between groups for SDNN and LF in all the periods, while for HF parameters the difference is statistically significant only in the night period. CONCLUSION: The use of the 24-h HRV method can provide more accurate and reproducible data than other conventional cardiovascular tests.

Aged↗
PubMed2001

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

The importance of endothelial nitric oxide (NO) generation in sustaining a tonic systemic vasodilatation is well established. Inhibiting NO production produces hypertension in animals and in humans and not surprisingly there has been considerable interest in establishing whether deficiencies of endothelial NO pathway activity are implicated in the aetiology of essential hypertension. The results of these investigations have been inconsistent with some suggestion that observed deficiencies of both basal and stimulated endothelial NO generation in hypertensive subjects may be an effect rather than the cause of raised arterial pressure. It is increasingly recognised that neuronal production of NO also influences cardiovascular homeostasis through its action as a neuromodulator within the autonomic nervous system. Overall NO has been shown to have sympatho-inhibitory and vagotonic effects, acting by both central and peripheral mechanisms. Sympathetic overactivity, coupled with the permissive role of a depressed level of baroreflex mediated cardiac vagal control, may play a significant role in the genesis of human hypertension. Early work in hypertensive rats suggests that neuronal NO production is impaired at a number of key central sites concerned with autonomic cardiovascular regulation. This data is consistent with the pattern of autonomic dysfunction observed in human hypertension. The possibility that neuronal rather than endothelial production of NO might play a significant role in the aetiology of essential hypertension is a promising area for future human research.

Autonomic Nervous System↗
PubMed1981

Microcomputer-based measurement of beat-to-beat intervals and analysis of heart rate variability.

This paper presents detailed information about a small, low-cost computerized system for on-line data processing which may easily be adapted to various problems. In the application described, the system operates as a heart detector and analyzer providing ECG signal filtering, measurement of beat-to-beat intervals (resolution: 1 ms), elimination of both artifacts and extrasystoles, and statistical analysis. All data and results are stored on magnetic tape and printed. This device proved to be a valuable tool in the investigation of heart rate abnormalities, which seem to indicate the presence of autonomic dysfunction observed in long-term diabetes mellitus. Preliminary results show that the decrease of normal beat-to-beat variation in diabetics is highly correlated with diabetic neuropathy and microangiopathy of the eye.

Autonomic Nervous System↗
PubMed1985

An hereditary sensory and autonomic neuropathy transmitted as an X-linked recessive trait.

Five members of a single family presented with neuropathic deformities and ulceration of the feet developing in the first and second decades of life, and progressed slowly over many years. In this form of hereditary sensory and autonomic neuropathy, there was minimal tendon reflex impairment, cutaneous sensory impairment was restricted to the feet, and there was no autonomic dysfunction. The only neurophysiological abnormality was that of reduced or absent sural nerve sensory action potentials. Sural nerve biopsies taken from two affected family members showed changes of a chronic neuropathy with loss of myelinated fibres, particularly affecting those of small diameter. Unmyelinated fibres were present in normal numbers. This condition differed from other forms of hereditary sensory and autonomic neuropathy having an X-linked recessive mode of inheritance.

Adolescent↗
PubMed1988

Neuritis cordis due to the acute polyneuritis of the Guillain-Barré syndrome.

Three patients with the Guillain-Barré syndrome which followed the course of Landry's acute ascending paralysis died a sudden cardiac death. Autonomic dysfunction had appeared clinically, consisting of sphincter disturbances in one patient and fluctuating blood pressure and bradycardia in the other. In a twenty-three year old female patient cardiac function had been inconspicuous, apart from tachycardia, but the ECG showed S-T segment depression and flat T waves. Postmortem examination revealed acute inflammatory demyelinating polyradiculoneuritis involving the peripheral autonomic nervous system and especially the nerves of the heart. Immunohistochemically, the inflammatory cell infiltrations of this neuritis cordis consisted of macrophages (MAC 387 positive) and T lymphocytes (UCHL1 positive). No indication of a direct viral infection of the inflamed cardiac nerves was detectable by immunohistochemistry (HSV, CMV, influenza virus) nor by electron microscopy. The neuritis cordis was classified as an inflammatory cardio-neuropathy secondary to a patchy acute polyneuritis of the Guillain-Barré syndrome, involving the autonomic nervous system. Myocarditis could be discounted, and the neuritis cordis was thought to be responsible for the sudden cardiac death.

Acute Disease↗
PubMed2001

Myasthenia gravis with autoimmune autonomic neuropathy.

The autoantibodies that impair neuromuscular junction transmission in myasthenia gravis are specific for the nicotinic acetylcholine receptor (AChR) of muscle. Antibodies specific for AChRs in ganglionic neurons are found in a majority of patients with subacute autonomic neuropathy. Dysautonomia is not a recognized feature of myasthenia gravis, but there have been rare reports of myasthenia gravis coexisting with autonomic failure, usually in association with thymoma. Here we report seven patients who had myasthenia gravis with subacute autonomic failure. Their autonomic dysfunction ranged from isolated gastroparesis to severe panautonomic failure. Gastrointestinal dysmotility was a common feature. All had antibodies against muscle AChR, and three (all of whom had thymoma) had antibodies against neuronal ganglionic AChRs. In several patients, gastrointestinal function improved clinically after administration of an acetylcholinesterase inhibitor. These observations support a rare but definite clinical association between myasthenia gravis and autonomic failure and strengthen the concept that subacute autonomic neuropathy is an autoimmune disorder.

Adult↗
PubMed2002

Autonomic nervous system function in Huntington's disease.

OBJECTIVE: To investigate whether Huntington's disease (HD) affects autonomic nervous system (ANS) functioning. METHODS: Twenty patients with HD who had positive genetic test results underwent standardised ANS function tests including sympathetic skin responses (SSRs) of the hands and feet, measurements of heart rate variability (HRV), both during five minutes of resting and deep respiration, and an orthostatic blood pressure test. Patients were classified according to the motor subscale of the unified Huntington's disease rating scale (UHDRS; mean (SD) score 26.4 (13.6)) and divided into two subgroups: UHDRS <25 points (early stages, E-HD) and UHDRS > or =25 points (mid stages, M-HD). Autonomic indices were compared with those obtained for a group of well matched healthy controls (n=60). RESULTS: Overall, patients showed lower HRV indices than controls. Multivariate analysis with the independent factor of "group" (controls, E-HD, M-HD) showed a significant group effect on both the high frequency power (F=4.32, p=0.017) and the coefficient of variation (F=4.23, p=0.018), indicating a significant reduction in vagal modulation in the M-HD group. There was a shift in autonomic neurocardiac balance towards sympathetic predominance in the M-HD group compared with controls (F=2.89, p=0.062). Moreover, we found an inverse correlation between the severity of clinical HD symptoms (assessed by the UHDRS) and the modulation of cardiovagal activity (p=0.028). Vagal dysregulation was present in two patients; one of them also showed a pathological blood pressure test and a latency prolongation in the SSRs of the hands. Two other patients had pathologically reduced SSR amplitudes. Only patients of the M-HD group were affected. CONCLUSION: Autonomic dysfunction is present even in the middle stages of HD and affects both the sympathetic and parasympathetic branch of the ANS.

Adult↗