BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy (CAA) is a major cause of lobar intracerebral hemorrhage and cognitive impairment and is associated with white matter hyperintensities and cerebral microbleeds. MRI diffusion tensor imaging detects microstructural tissue damage in advanced CAA even in areas that appear normal on conventional MRI. We hypothesized that higher global mean apparent diffusion coefficient (mean ADC), reflecting a higher amount of chronic tissue disruption caused by CAA, would be independently associated with CAA-related cognitive impairment. METHODS: Preintracerebral hemorrhage cognitive impairment was systematically assessed using a standardized questionnaire (IQCODE) in 49 patients. Volume of white matter hyperintensities, number of microbleeds, and mean ADC were determined from MRIs obtained within 14.0+/-22.5 days of intracerebral hemorrhage cognitive impairment. White matter hyperintensities and mean ADC were measured in the hemisphere uninvolved by intracerebral hemorrhage to avoid confounding. RESULTS: Preintracerebral hemorrhage cognitive impairment was identified in 10 of 49 subjects. Mean ADC was the only variable associated with preintracerebral hemorrhage cognitive impairment and was elevated in those with preintracerebral hemorrhage cognitive impairment compared with those without (12.4x10(-4) versus 11.7x10(-4) mm(2)/s; P=0.03). Mean ADC positively correlated with age but not white matter hyperintensities or number of microbleeds. In logistic regression controlling for age and visible cerebral atrophy, mean ADC was independently associated with preintracerebral hemorrhage cognitive impairment (OR per 1x10(-4) mm(2)/s increase=2.45, 95% CI 1.11 to 5.40, P=0.04). CONCLUSIONS: Mean ADC is independently associated with preintracerebral hemorrhage cognitive impairment in CAA. The lack of correlation with other MRI markers of CAA suggests that mean ADC may be sensitive to distinct aspects of CAA pathology and its tissue consequences. These results suggest that global MRI diffusion changes are sensitive to clinically relevant microstructural alterations and may be useful markers of CAA-related tissue damage.
BACKGROUND AND PURPOSE:Cerebral amyloid angiopathy (CAA) is a major cause of lobar intracerebral hemorrhage and cognitive impairment and is associated with white matter hyperintensities and cerebral microbleeds. MRI diffusion tensor imaging detects microstructural tissue damage in advanced CAA even in areas that appear normal on conventional MRI. We hypothesized that higher global mean apparent diffusion coefficient (mean ADC), reflecting a higher amount of chronic tissue disruption caused by CAA, would be independently associated with CAA-related cognitive impairment. METHODS:Preintracerebral hemorrhage cognitive impairment was systematically assessed using a standardized questionnaire (IQCODE) in 49 patients. Volume of white matter hyperintensities, number of microbleeds, and mean ADC were determined from MRIs obtained within 14.0+/-22.5 days of intracerebral hemorrhage cognitive impairment. White matter hyperintensities and mean ADC were measured in the hemisphere uninvolved by intracerebral hemorrhage to avoid confounding. RESULTS:Preintracerebral hemorrhage cognitive impairment was identified in 10 of 49 subjects. Mean ADC was the only variable associated with preintracerebral hemorrhage cognitive impairment and was elevated in those with preintracerebral hemorrhage cognitive impairment compared with those without (12.4x10(-4) versus 11.7x10(-4) mm(2)/s; P=0.03). Mean ADC positively correlated with age but not white matter hyperintensities or number of microbleeds. In logistic regression controlling for age and visible cerebral atrophy, mean ADC was independently associated with preintracerebral hemorrhage cognitive impairment (OR per 1x10(-4) mm(2)/s increase=2.45, 95% CI 1.11 to 5.40, P=0.04). CONCLUSIONS: Mean ADC is independently associated with preintracerebral hemorrhage cognitive impairment in CAA. The lack of correlation with other MRI markers of CAA suggests that mean ADC may be sensitive to distinct aspects of CAA pathology and its tissue consequences. These results suggest that global MRI diffusion changes are sensitive to clinically relevant microstructural alterations and may be useful markers of CAA-related tissue damage.
Authors: H C O'Donnell; J Rosand; K A Knudsen; K L Furie; A Z Segal; R I Chiu; D Ikeda; S M Greenberg Journal: N Engl J Med Date: 2000-01-27 Impact factor: 91.245
Authors: H Chabriat; S Pappata; C Poupon; C A Clark; K Vahedi; F Poupon; J F Mangin; M Pachot-Clouard; A Jobert; D Le Bihan; M G Bousser Journal: Stroke Date: 1999-12 Impact factor: 7.914
Authors: E E Smith; D H Salat; J Jeng; C R McCreary; B Fischl; J D Schmahmann; B C Dickerson; A Viswanathan; M S Albert; D Blacker; S M Greenberg Journal: Neurology Date: 2011-04-26 Impact factor: 9.910
Authors: Gregory A Dierksen; Maureen E Skehan; Muhammad A Khan; Jed Jeng; R N Kaveer Nandigam; John A Becker; Ashok Kumar; Krista L Neal; Rebecca A Betensky; Matthew P Frosch; Jonathan Rosand; Keith A Johnson; Anand Viswanathan; David H Salat; Steven M Greenberg Journal: Ann Neurol Date: 2010-10 Impact factor: 10.422
Authors: Andreas Charidimou; Gregoire Boulouis; M Edip Gurol; Cenk Ayata; Brian J Bacskai; Matthew P Frosch; Anand Viswanathan; Steven M Greenberg Journal: Brain Date: 2017-07-01 Impact factor: 13.501
Authors: Oliver J Standring; Jacob Friedberg; Yorghos Tripodis; Alicia S Chua; Jonathan D Cherry; Victor E Alvarez; Bertrand R Huber; Weiming Xia; Jesse Mez; Michael L Alosco; Raymond Nicks; Ian Mahar; Morgan J Pothast; Hannah M Gardner; Gaoyuan Meng; Joseph N Palmisano; Brett M Martin; Brigid Dwyer; Neil W Kowall; Robert C Cantu; Lee E Goldstein; Douglas I Katz; Robert A Stern; Ann C McKee; Thor D Stein Journal: Acta Neuropathol Date: 2019-06-10 Impact factor: 17.088