Postural neurocognitive and neuronal activated cerebral blood flow deficits in young chronic fatigue syndrome patients with postural tachycardia syndrome

Departments of Physiology, New York Medical College, Valhalla, New York. USA.
AJP Heart and Circulatory Physiology (Impact Factor: 4.01). 12/2011; 302(5):H1185-94. DOI: 10.1152/ajpheart.00994.2011
Source: PubMed

ABSTRACT Neurocognition is impaired in chronic fatigue syndrome (CFS). We propose that the impairment relates to postural cerebral hemodynamics. Twenty-five CFS subjects and twenty control subjects underwent incremental upright tilt at 0, 15, 30, 45, 60, and 75° with continuous measurement of arterial blood pressure and cerebral blood flow velocity (CBFV). We used an n-back task with n ranging from 0 to 4 (increased n = increased task difficulty) to test working memory and information processing. We measured n-back outcomes by the number of correct answers and by reaction time. We measured CBFV, critical closing pressure (CCP), and CBFV altered by neuronal activity (activated CBFV) during each n value and every tilt angle using transcranial Doppler ultrasound. N-back outcome in control subjects decreased with n valve but was independent of tilt angle. N-back outcome in CFS subjects decreased with n value but deteriorated as orthostasis progressed. Absolute mean CBFV was slightly less than in control subjects in CFS subject at each angle. Activated CBFV in control subjects was independent of tilt angle and increased with n value. In contrast, activated CBFV averaged 0 in CFS subjects, decreased with angle, and was less than in control subjects. CCP was increased in CFS subjects, suggesting increased vasomotor tone and decreased metabolic control of CBFV. CCP did not change with orthostasis in CFS subjects but decreased monotonically in control subjects, consistent with vasodilation as compensation for the orthostatic reduction of cerebral perfusion pressure. Increasing orthostatic stress impairs neurocognition in CFS subjects. CBFV activation, normally tightly linked to cognitive neuronal activity, is unrelated to cognitive performance in CFS subjects; the increased CCP and vasomotor tone may indicate an uncoupling of the neurovascular unit during orthostasis.

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Available from: Julian Stewart, Feb 17, 2015
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    • "Panerai and colleagues (2005) found other tests, the critical closing pressure (CCP) and resistance area product (RAP), to be better measures of cerebral blood flow responses induced by mental activation tasks rather than cerebrovascular resistance alone. Stewart et al. (2012) has found increasing orthostatic stress impairs cognitive functioning in CFS/POTS. However, these impairments are not related to cerebral blood flow using cerebrovascular resistance alone, but when CCP and RAP were used, cerebral blood flow was related to neurocognitive abilities. "
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    ABSTRACT: Chronic fatigue syndrome (CFS) is characterized by fatigue, sleep dysfunction, and cognitive deficits (Fukuda et al., 1994). Research surrounding cognitive functioning among patients with CFS has found difficulty with memory, attention, and information processing. A similar disorder, postural tachycardia syndrome (POTS), is characterized by increased heart rate, fatigue, and mental cloudiness (Raj et al., 2009). Potential implications of cognitive deficits for patients with CFS and/or POTS are discussed, including difficulties with school and/or employment. A few biological theories (i.e., kindling, impairments in the central nervous system, and difficulty with blood flow) have emerged as potential explanations for the cognitive deficits reported in both CFS and POTS Future research should continue to examine possible explanations for cognitive impairments in CFS and POTS, and ultimately use this information to try and reduce cognitive impairments for these patients.
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    ABSTRACT: In this issue of the Journal of Internal Medicine, Lewis and colleagues [1] provide compelling data for a novel subgroup within the chronic fatigue syndrome (CFS) population. They show that approximately 13% (24/179) of CFS patients have postural orthostatic tachycardia syndrome (POTS), a form of dysautonomia implying that when patients change their body position from supine to upright, their heart rate will increase abnormally (tachycardia). POTS is associated with several symptoms often seen in CFS patients: fatigue, lightheadedness, dizziness, neurocognitive deficits and exercise intolerance. Importantly, this was a confirmatory study of a previously published pilot study that found a prevalence rate for POTS of 29% in a smaller sample (n=63) of CFS patients [2]. Another significant finding is the differences in fatigue severity, depressive thoughts, and daytime hypersomnolence between CFS patients with and without POTS, providing evidence for the clinical importance of POTS in CFS. © 2013 The Association for the Publication of the Journal of Internal Medicine.
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    ABSTRACT: Syncope from sustained orthostasis results from cerebral hypoperfusion associated with reductions in arterial pressure at the level of the brain (BP(MCA)) and reductions in arterial CO(2) as reflected by end-tidal values (P(ET)CO(2)). It was hypothesized that reductions in P(ET)CO(2) increase cerebrovascular tone prior to a drop in BPMCA that ultimately leads to syncope. Twelve men (21-42 years of age) completed an orthostatic tolerance test consisting of head up tilt and progressive lower body negative pressure, before and after completing five days of continuous head-down bed rest (HDBR). Cerebral blood velocity (CBFV), BP(MCA), and P(ET)CO(2) were continuously recorded throughout the test. Cerebrovascular indicators: cerebrovascular resistance (CVRi), critical closing pressure (CrCP), and resistance area product (RAP) were calculated. Comparing from supine baseline to 6-10min after the start of tilt there were reductions in CBFV, P(ET)CO(2), BPMCA, and CrCP, an increase in RAP, and no change in CVRi. Over the final 15 min prior to syncope in the pre-HDBR tests, CBFV and CrCP were significantly related to changes in P(ET)CO(2) (r=0.69±0.17, and r=0.63±0.20 respectively), and BPMCA, which was not reduced until the last minute of the test, correlated with a reduction in RAP (r=0.91±0.09). Post-HDBR, tilt tolerance was markedly reduced and changes in CBFV were dominated by a greater reduction in BP(MCA) with no relationships to P(ET)CO(2). Therefore, pre-HDBR, changes in P(ET)CO(2) with orthostasis contributed to increases in cerebrovascular tone and reductions in CBFV during the progression toward syncope whereas after five days of HDBR orthostatic responses were dominated by changes in BP(MCA).
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