Autonomic dysfunction as the presenting feature of Guillain-Barré syndrome.

Autonomic dysfunction has been demonstrated in various conditions associated with peripheral neuropathy such as acute intermittent porphyria, amyloidosis, and Guillain-Barré syndrome (GBS). In the latter, hypertension is an associated complication that typically occurs after neurological signs are already present. We report a case of a patient with autonomic dysfunction as the presenting feature who was admitted to the coronary unit with chest pain and hypertension. Subsequently, he developed progressive symmetric muscle, weakness, sensory changes, and areflexia. GBS was then diagnosed based on the clinical picture, albuminocytologic dissociation in the cerebrospinal fluid, and electrodiagnostic abnormalities suggestive of demyelinative polyneuropathy with conduction block. Few cases in the literature have reported autonomic dysfunction as the presenting feature of GBS, such as in this case. In a previously asymptomatic patient, acute onset of autonomic dysfunction should alert the physician to the possibility of an acute polyneuropathy, such as GBS.

Regulation of alpha and beta components of noradrenergic cyclic AMP response in cortical slices.

The cyclic AMP response to catecholamines in the rat cerebral cortex is mediated by both beta- and alpha-adrenoceptors. The beta-receptors cause a direct activation of adenylate cyclase whereas the alpha alpha-receptors play a modulatory role and act by potentiating the response to beta stimulation. The present study investigated whether the functions of these two types of cyclic AMP-linked receptors are regulated differently by various physiological factors known to affect adrenoceptor function. It was found that treatments that affect central noradrenergic neuronal function including repeated administration of desmethylimipramine or lesion of central noradrenergic pathways produced selective changes in the cAMP response to beta-receptor stimulation whereas treatments that affect adrenocortical function including ACTH of corticosterone administration and hypophysectomy or adrenalectomy produced selective changes in the potentiation response to alpha-receptor stimulation. The change in the alpha potentiation effect caused by corticosterone was found to be abolished in the presence of prazosin indicating that the hormone affects alpha 1-adrenoceptor function. The results support the hypothesis that the beta response in the cortex is under the control of the noradrenergic system while the alpha potentiation response is under the control of the adrenocortical system.

Alpha-adrenergic modulation of cyclic AMP formation in rat CNS: highest level in olfactory bulb.

The cyclic adenosine monophosphate response to catecholamines in the rat brain is mediated by beta-adrenergic receptors which activate adenylate cyclase and by alpha-adrenergic receptors which potentiate the response to beta-stimulation. We have found that the alpha-potentiation effect in the olfactory bulb is 2-3X greater than in other forebrain areas. This correlates with the extremely high density of alpha-receptors in this brain region and makes it a useful model for the study of alpha-receptor function.

Effect of repeated restraint stress, desmethylimipramine or adrenocorticotropin on the alpha and beta adrenergic components of the cyclic AMP response to norepinephrine in rat brain slices.

The cyclic AMP response to catecholamines in rat cortical slices is mediated by a beta adrenergic receptor which is coupled to adenylate cyclase and an alpha adrenergic receptor which potentiates the response to beta receptor stimulation. The present studies examined the effects of repeated restraint stress, adrenocorticotropin or desmethylimipramine administration on the beta and alpha adrenergic components of this response. Restraint was found to produce a small nonsignificant decrease of the beta receptor response accompanied by a significant reduction of the alpha receptor-induced potentiation of the beta response. Desmethylimipramine was found to lower the cyclic AMP response to beta receptor stimulation but not to alter the alpha-induced potentiation of the beta response. Adrenocorticotropin, like restraint stress, was found to reduce only the alpha-induced potentiation of the beta response. Experiments with adenosine and histamine showed that restraint stress lowered the alpha-induced potentiation of cyclic AMP responses to these neurohormones also. It is concluded that restraint stress acts primarily to reduce the response to stimulation of central alpha adrenergic receptors whereas desmethylimipramine acts primarily to reduce the response to stimulation of beta adrenergic receptors. Adrenocorticotropin has the same effect as restraint stress suggesting that pituitary adrenal hormones mediate the stress effect.