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Autonomic dysfunction

Dysautonomia is any disease or malfunction of the autonomic nervous system. This includes postural orthostatic tachycardia syndrome (POTS), neurocardiogenic syncope, mitral valve prolapse dysautonomia, pure autonomic failure, multiple system atrophy (Shy-Drager syndrome), and a number of lesser-known disorders. more...

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In some cases, dysautonomia results in a reduction in the ability of the heart and circulatory system to compensate for changes in posture, causing dizziness or syncope (fainting) when one, eg, stands suddenly. In other cases, the heart may race (tachycardia) for no apparent reason, or the kidneys may fail to properly retain water (diabetes insipidus).

The effects of dysautonomia may be minor, only limiting the patient's activities slightly, or they may be totally disabling, leaving the patient bedridden. Chronic fatigue syndrome is often associated with dysautonomia.

History

In the nineteenth and earlier twentieth centuries, a diagnosis that was almost solely given to women was called "neurasthenia," or a "weak nervous system." These women would present symptoms of fatigue, weakness, dizziness and fainting, and the doctor's orders would simply be bed rest. Some of these women died, while many others recovered. No one understood where the problems came from.

Nowadays, diagnostic criteria and treatment for various forms of dysautonomia have sharpened, and doctors have realized that some men have it, too.

Treatment

There is no cure for dysautonomia. Secondary forms may improve with treatment of the underlying disease. In many cases treatment of primary dysautonomia is symptomatic and supportive. Measures to combat orthostatic hypotension include elevation of the head of the bed, frequent small meals, a high-salt diet, and drugs such as fludrocortisone, midodrine, and ephedrine.

Prognosis

The outlook for patients with dysautonomia depends on the particular diagnostic category. Patients with chronic, progressive, generalized dysautonomia in the setting of central nervous system degeneration have a generally poor long-term prognosis. Death can occur from pneumonia, acute respiratory failure, or sudden cardiopulmonary arrest in such patients.

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Autonomic denervation in the experimental American trypanosomiasis in rats: Functional response to neurotoxins
From Revista do Instituto de Medicina Tropical de Sao Paulo, 5/1/02 by Junior, Antonio Lucio teixeira

SUMMARY OF THESIS*

A well documented feature of Chagas disease is an extensive reduction in number of neuronal cell bodies in cardiac parasympathethic ganglia, and oesophageal and colonic myenteric plexus. This autonomic denervation has been suggested to play a role in the development of the late manifestations of Cha-as disease, i.e. dilated cardiomyopathy, megacolon and megaoesophagus. Severe cardiac autonomic denervation also occurs in the acute experimental American trypanosomiasis in rats. The present study aims at verifying whether this denervation, as demonstrated histochemically, was accompanied by impairment of heart function, as assessed by the chronotropic response to the scorpionic (Tit)l,ts serrulatus) crude venom in the isolated rat heart preparation.

The venom extracted from the scorpion Tityus serrulatus contains potent neurotoxins that activate sodium channels in neuronal terminals leading to the release of the mediators acetylcholine and noradrenaline. We have shown that activation of isolated heart preparation (Langendorff's) with T serrulatus venom induces a marked rhythm alteration characterised by significant early bradycardia followed by tachycardia which were blocked by muscarinic and b,-adrenoceptor antagonists, respectively. Thus, T serrulatus venom is a useful tool to evaluate chronotropic response of adrenergic and cholinergic nerve terminals in isolated rat heart preparation.

In control hearts, the venom induced significant bradycardia (73% decrease in heart rate) followed by tachycardia (10% increase in heart rate). In infected animals, despite the severe (sympathetic) or moderate (parasympathetic) cardiac denervation, the venom provoked similar bradycardia (63% decrease), but the tachycardia was higher (50% increase). The basal heart rate of infected animals (164 15 bpm, beats per minute) was significantly lower compared to control rats (213 +/- 13 bpm). Atropine prevented this lower rate in infected animals. Our results demonstrated minor cardiac sympathetic dysfunction with sparing of the parasympathetic function.

Altogether, our present and previous studies in rats, and the evidence of progressive autonomic denervation in chronic chagasic cardiomyopathy favour the notion that autonomic denervation may be a consequence and not the cause of the chronic Chagas heart disease.

*This thesis is available at the Library of the Instituto de Medicina Tropical de Sio Paulo

TEIXEIRA Jr., Antonio Lucio - Desnervacao autonomica cardiaca na tripanosomfase americana experimental em ratos: resposta funcional a neurotoxinas. Belo Horizonte, 2000. (Dissertaqao de mestrado - Instituto de Ciencias Biol6gicas da Universidade Federal de Minas Gerais)

Antonio Lucio Teixeira Junior Rua Sdo Joao da Ponte 157/201 30310-650 Belo Horizonte - MG altexjr@hotmail.com

Copyright Instituto de Medicina Tropical de Sao Paulo May/Jun 2002
Provided by ProQuest Information and Learning Company. All rights Reserved

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