Another feature of VVS is cardiac asystole, which has a variable incidence, ranging from 9.1 to 24% ( 12, 14). In a retrospective review in 226 individuals with syncope during HUTT, 5.8% of patients had seizures ( 13). Up to 91% of individuals with syncope may develop a rigid posture and have some myoclonic jerking activity while about 6–25% of individuals with vasodepressive syncope may have convulsive episodes ( 11, 12). The co-occurrence of VVS and seizures and/or cardiac asystole, that is, “complex VVS,” is well-known though the underlying pathophysiology remains unclear. The HUTT is also useful in distinguishing different types of VVS. HUTT can differentiate between symptomatic and asymptomatic patients ( 9), reflex syncope, orthostatic hypotension, and pseudosyncope and has been estimated to have a sensitivity of 65% and a specificity of 92% ( 8, 10). By tilting a patient between 60 and 90°, orthostatic stress and sympathetic activity are maximal ( 8). in 1945 ( 7), is the gold standard for diagnosing syncope. Head-up tilt table (HUTT) testing, first described by Allen et al. Normally, during standing 300–800 mL of blood pools in the lower limbs, inducing baroreceptor reflexes, encouraging sympathetic activation and maintenance of blood pressure ( 4).
Providing orthostatic challenge can be a useful technique for diagnosing VVS. It is common for patients that undergo VVS to have “pre-syncopal” phase or prodrome, which can include nausea, light headedness, blurry vision, or pallor. While reflex syncope may be caused by dysfunction in either parasympathetic or sympathetic efferent pathways, autonomic efferents remain largely intact ( 6). While VVS may, at times, be homeostatically protective ( 5), the most prevalent form is debilitating syncope ( 2– 4) and results from abnormal cardiovascular reflexes that cause vasodilation, bradycardia, and a resulting fall in systolic blood pressure and hypoperfusion of the brain. By doing so, it can significantly increase direct and indirect social healthcare costs. Syncope can have serious adverse effects on quality of life by reducing mobility and usual activities and by increasing depression, pain, and risk of physical injury. The estimates of syncope range from 18.1 to 39.7 episodes per 1,000 patients per year, but this incidence significantly increases after the age of 70 years ( 4). Vasovagal syncope (VVS) may be described as a “transient loss of consciousness and postural tone resulting from global cerebral hypoperfusion with spontaneous and complete recovery and no neurological sequelae” ( 1– 3). Seizures had multiple distinguishing features from those typically associated with epileptic seizures.Ĭonclusions: The underlying pathophysiologic mechanisms of complex VVS remain unclear, but the severity of cerebral hypoperfusion due to bradycardia likely plays a key role in seizure generation. Autonomic abnormalities were frequent but did not distinguish the two VVS subgroups. The severity of bradycardia significantly correlated with complex VVS and was a predictor of SySz. Mean asystole duration was somewhat longer in the SyAsSz group. Males were significantly more likely to have complex VVS. Eighteen (23%) were complex VVS five had an associated seizure (SySz), nine were accompanied by asystole (SyAs), and four had both (SySzAs). Vasodepressor (45%) and mixed (38%) VVS were the most prevalent types. Results: A total of 78 independent VVS were recorded in 60 patients of which 24% were not preceded by presyncope. Simple frequency and correlation analysis were performed using the ANOVA.
The following variables were recorded: cardiovascular indices during HUTT, autonomic testing results, and semiology of asystole and/or seizure when present. Methods: We reviewed medical records of all patients who were referred for orthostatic intolerance and had a definite VVS during the head-up tilt table testing (HUTT).
Objective: To further characterize VVS and to find predictive features of “complex” VVS (defined as VVS associated with seizures and/or asystole). Seizure and/or asystole may accompany VVS, though their prediction within the VVS cohort remains elusive. Division of Neurology, Department of Medicine, University of Alberta, Edmonton, AB, Canadaīackground: Vasovagal syncope (VVS) occurs due to cerebral hypoperfusion from a fall in blood pressure, with accompanying bradycardia in most cases.Anwer Zohaib Siddiqi, Derrick Blackmore and Zaeem Azfer Siddiqi *
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