PubMed Health⌕ Search

PubMed · 9333978

[Syncopes from the neurologic viewpoint].

Abstract

A syncope is defined as a sudden, temporary loss of consciousness, associated with loss of postural tone with spontaneous recovery. The incidence is high and the differential diagnosis broad; therefore, the first observations are essential for the management of the patient. In this review diseases will be described which manifest themselves with syncopes that fall under the auspices of either internal medicine or neurology. First, the etiologies of syncopes are discussed in the strict sense of the word, i.e. due to a global cerebral ischemia such as in orthostatic hypotension and vasopressor syncopes. Thereafter, a discussion concerning the differential diagnosis of syncopes will be introduced, including mainly psychogenic and epileptic seizures as well as vertebrobasilar hypoperfusion. Depending on the reason of the loss of consciousness, it can be a common benign disorder or a severe life-threatening disease. The personal history or witness account of the incidence provides the most useful information concerning diagnosis. The cardiological diagnostic procedures are discussed elsewhere. In some instances an EEG can further help with the diagnosis. In many cases an etiology can't be found, even if extensive investigations have been performed.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Scollo-Lavizzari, J Lechner-Scott. 1997. [Syncopes from the neurologic viewpoint].. https://pubmed.ncbi.nlm.nih.gov/9333978/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Idiopathic congenital central hypoventilation syndrome: evaluation of brain-derived neurotrophic factor genomic DNA sequence variation.

Idiopathic congenital central hypoventilation syndrome (CCHS) is an unique disorder of respiratory control, occurring in association with Hirschsprung disease (HSCR), tumors of neural crest origin, and symptoms of autonomic nervous system dysfunction (ANSD). CCHS is thought to be genetic in origin based upon 1) affected sib pairs, 2) genetic analysis, and 3) identification of genetic mutations in both HSCR and CCHS patients. Because these mutations have been found in but a few cases of CCHS, exploration of other candidate genes has continued. Brain-derived neurotrophic factor (BDNF) represents a potential candidate gene to consider because of altered respiratory control in the BDNF knock-out mouse model and localization to the enteric nervous system in human tissue. The objective of this study was to determine the frequency of BDNF mutations among 19 children with CCHS (five with HSCR) compared to 40 unaffected unrelated controls. Using the known genomic DNA sequence for BDNF, polymerase chain reaction (PCR)-amplified genomic DNA was analyzed by standard sequencing methods. A discrete mutation was identified in one of 19 children with isolated CCHS and the unaffected father. Specifically, an isoleucine was substituted for a threonine or serine in the amino acid sequence. Absence of this mutation in 40 controls confirmed that this mutation was likely not a common polymorphism. These data further support a genetic basis for CCHS, though mutations of BDNF are not consistent in this disorder.

Autonomic Nervous System Diseases↗

Cirrhotic cardiomyopathy: a pathophysiological review of circulatory dysfunction in liver disease.

The systemic circulation in patients with cirrhosis is hyperdynamic with an increased cardiac output and heart rate and a reduced systemic vascular resistance as the most pronounced alterations. The concomitant cardiac dysfunction has recently been termed "cirrhotic cardiomyopathy", which is an entity different from that seen in alcoholic heart muscle disease. Clinically, these patients present with sodium fluid retention and strain often unmasks the presence of latent heart failure. No specific treatment can yet be recommended but caution should be used with respect to procedures that may stress the heart such as shunt implantation and liver transplantation.

Autonomic Nervous System Diseases↗

Nocturnal hypoxemia: a neglected cardiovascular risk factor in end-stage renal disease?

Its is well established that sleep apnea (SA) is a health problem of paramount importance because it disrupts sleep and quality of life and may induce serious neuroendocrine and cardiovascular complications. There is little doubt that chronic renal failure is an independent cause of SA. The hypothesis that SA may depend on the accumulation of endogenous opioids still remains to be tested. Cytokines, particularly TNF-alpha and IL-6 which are much elevated in end-stage renal disease (ESRD), may also be implicated in the pathogenesis of SA. Nocturnal hypoxemia is an independent predictor of cardiovascular events in ESRD and the prediction power of this parameter remains strong and substantially unmodified after statistical adjustment for established cardiovascular risk factors in the dialysis population. Left ventricular hypertrophy and dysautonomia appear to be most likely intermediate mechanisms mediating the adverse cardiovascular effects of SA in ESRD.

Autonomic Nervous System Diseases↗