ramakentesh
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Another one from Dr Julian Stewart:
http://www.ncbi.nlm.nih.gov/pubmed/22180650
Postural Neurocognitive and Neuronal Activated Cerebral Blood Flow Deficits in Young Chronic Fatigue Syndrome Patients with Postural Tachycardia Syndrome.
Neurocognition is impaired in Chronic Fatigue Syndrome (CFS). We propose that impairment relates to postural cerebral hemodynamics. 25 CFS and 20 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 and every tilt angle using transcranial Doppler ultrasound. N-Back outcome in controls decreased with N but was independent of tilt angle. N-Back outcome in CFS decreased with N but deteriorated as orthostasis progressed. Absolute mean CBFv was slightly less than control in CFS at each angle. Activated CBFv in controls was independent of tilt angle and increased with N. In contrast, activated CBFv averaged 0 in CFS, decreased with angle and was less than control. CCP was increased in CFS suggesting increased vasomotor tone and decreased metabolic control of CBFv. CCP did not change with orthostasis in CFS, 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. CBFv activation, normally tightly linked to cognitive neuronal activity, is unrelated to cognitive performance in CFS; increased CCP and vasomotor tone may indicate uncoupling of the neurovascular unit during orthostasis
http://www.ncbi.nlm.nih.gov/pubmed/22180650
Postural Neurocognitive and Neuronal Activated Cerebral Blood Flow Deficits in Young Chronic Fatigue Syndrome Patients with Postural Tachycardia Syndrome.
Neurocognition is impaired in Chronic Fatigue Syndrome (CFS). We propose that impairment relates to postural cerebral hemodynamics. 25 CFS and 20 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 and every tilt angle using transcranial Doppler ultrasound. N-Back outcome in controls decreased with N but was independent of tilt angle. N-Back outcome in CFS decreased with N but deteriorated as orthostasis progressed. Absolute mean CBFv was slightly less than control in CFS at each angle. Activated CBFv in controls was independent of tilt angle and increased with N. In contrast, activated CBFv averaged 0 in CFS, decreased with angle and was less than control. CCP was increased in CFS suggesting increased vasomotor tone and decreased metabolic control of CBFv. CCP did not change with orthostasis in CFS, 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. CBFv activation, normally tightly linked to cognitive neuronal activity, is unrelated to cognitive performance in CFS; increased CCP and vasomotor tone may indicate uncoupling of the neurovascular unit during orthostasis