Reaction time and brain disease: relations to location, etiology and progression of cerebral dysfunction

Abstract

Using the results from 485 patients with various forms of cerebral dysfunctions and from 60 hospitalized controls, it was shown that measurement of continuous reaction times (CRT) is sensitive to cerebral lesions. Reaction times were more impaired by progressive than by non-progressive brain diseases. The test did not distinguish between patients with right-or left-hemisphere lesions and was not influenced either by etiology, chronicity, age or sex.Our conclusion is that CRT is useful as a "screening" test for the presence of cerebral dysfunction and is especially sensitive to progressive diseases. Its discrimination power is equivalent to more sophisticated and complex psychological tests.

Hepatic encephalopathy is associated with decreased cerebral oxygen metabolism and blood flow, not increased ammonia uptake

“…This included a continuous reaction time test (CRT) 13 to ensure that patients examined after recovery from HE and the control patients did not have minimal HE; the CRT could not be performed in three of the patients with HE grade III.…”

“…11 The model includes clearance of 13 N-ammonia from blood to brain tissue (K 1 ; mL blood/mL brain tissue/min), backflux of 13 N-ammonia from brain tissue to blood (k 2 ; per minute), and conversion of 13 N-ammonia to 13 N-glutamine in brain (k 3 ; per minute). 13 N-urea formed in the liver was assumed to enter and leave brain tissue by free diffusion and 13 N-glutamine in blood was assumed not to enter the brain tissue in any significant amount.…”

“…Blood radioactivity concentrations were measured using a well counter (Packard Instruments, Meriden, CT) that was cross-calibrated with the PET camera and concentrations were corrected for radioactive decay back to the start of the scan. Additional arterial blood samples of 2 mL were collected at 1, 2, 3, 5, 7, 10, 15, 20, 25, and 30 minutes after 13 N-ammonia administration for determination of blood concentrations of 13 N-ammonia, 13 N-urea, and 13 N-glutamine. 17 Analysis of PET Data.…”

“…For analysis of the 13 N-ammonia PET data, a brain tissue radioactivity concentration time-course was generated using the same VOI as for the 15 O-oxygen data. Kinetic parameters of cerebral 13 N-ammonia uptake and metabolism were calculated by nonlinear fitting of a two-tissue compartmental model of 13 N-ammonia uptake and metabolism to the 13 N-radioactivity concentration time-courses in brain tissue and arterial blood. 11 The model includes clearance of 13 N-ammonia from blood to brain tissue (K 1 ; mL blood/mL brain tissue/min), backflux of 13 N-ammonia from brain tissue to blood (k 2 ; per minute), and conversion of 13 N-ammonia to 13 N-glutamine in brain (k 3 ; per minute).…”

“…Kinetic parameters of cerebral 13 N-ammonia uptake and metabolism were calculated by nonlinear fitting of a two-tissue compartmental model of 13 N-ammonia uptake and metabolism to the 13 N-radioactivity concentration time-courses in brain tissue and arterial blood. 11 The model includes clearance of 13 N-ammonia from blood to brain tissue (K 1 ; mL blood/mL brain tissue/min), backflux of 13 N-ammonia from brain tissue to blood (k 2 ; per minute), and conversion of 13 N-ammonia to 13 N-glutamine in brain (k 3 ; per minute). 13 N-urea formed in the liver was assumed to enter and leave brain tissue by free diffusion and 13 N-glutamine in blood was assumed not to enter the brain tissue in any significant amount.…”