Time course of the apparent diffusion coefficient after cerebral infarction

Abstract

The purpose of this study was to evaluate quantitative apparent diffusion changes in the center of infarction by measurement of the apparent diffusion coefficient (ADC), and to investigate the influence of ischemia on the contralateral hemisphere. By diffusion echo-planar imaging (EPI) 52 patients showing cerebral infarction were studied within 5 h to >12 months after onset of clinical symptoms. Using three diffusion gradient strengths (b1=30 s/mm(2); b2=300 s/mm(2), b3=1100 s/mm(2)) ADC maps were generated. After onset of ischemia, ADC in the center of infarction was lower than in the contralateral regions of human brain. At first ADC declined for approximately 28 h to a minimum of approximately 150x10(-8) cm(2)/s. Then the ADC reincreased and reached a "pseudonormalization" after approximately 5 days. Chronic infarctions did show much higher ADC values (2000x10(-8) cm(2)/s) than unaffected areas. Neither localization nor size of infarctions showed a significant influence on this time course. In the center of infarction diffusion is isotropic. Even brain regions of the contralateral hemisphere are influenced by cerebral ischemia. In these regions ADC is higher than for physiological conditions. The ADC also declines especially for the first 2-3 days after onset of symptoms, also followed by reincrease. The ADC calculation enables determination of the onset of infarction more exactly than is possible using only diffusion-weighted imaging. Diffusion in the center of infarction is isotropic; hence, orientation of the diffusion gradients has no significant influence on sensitivity of measurements. The calculation of the ADC ratio based on data derived from the center of infarction and the contralateral hemisphere seems to be critical because the ADC in the unaffected contralateral hemisphere also changes.

Assessment of paramedian thalamic infarcts: MR imaging, clinical features and prognosis

“…However, occlusion of peripheral arteries in the PCA territory as well as of the thalamoperforating arteries may be a likely consequence caused by fragments of thrombotic material [27,40]. The results in the present study underline the necessity of additional DWI in detecting small ischemic lesions in the posterior circulation [41,42].…”

MRI of hyperacute stroke in the AChA territory

“…Only Beevor [1] and Alexander [3] have considered an AChA supply of the posteroventral crest of the putamen, and the former is to date the only anatomist to have described a cranial extension of AChA branches into the corona radiata. Contradictory results regarding the involvement of the corona radiata in AChA infarction are reported in the literature [16,17,19,24,31,32]. Clinical-pathological correlations in previous decades highlighted the fact that the combination of ipsilateral visual disturbance (homonymous hemianopsia or quadrantanopsia) with low to severe contralateral motor and/or sensory deficit was a highly suggestive clinical feature of AChA involvement [14].…”

“…Hypoesthetic ataxic hemiparesis has also been reported in this condition [14]. CT and MRI are the two major imaging modalities used for the diagnosis of acute ischemic stroke [15][16][17]. Frisen and colleagues first showed the CT appearance of ischemia involving the AChA territory [18].…”

Longitudinal Investigations on the Anterograde and Retrograde Degeneration in the Pyramidal Tract following Pontine Infarction with Diffusion Tensor Imaging

“…As a result, neural cells and axons at the infarct site undergo cytotoxic edema, which in turn restricts water molecule movement. In the subacute stage, with the cell lysis and the loss of normal tissue architecture, the freedom of water molecule diffusion increases [19,20,21]. Correspondingly, MD increases following the subacute stage.…”