C Gymnopoulos | PubMed Health

PubMed1998

Preliminary clinical-radiological assessment of a MR tissue signature model in human stroke.

We evaluated the ability of an MR signature model (SM) of cerebral ischemic injury to stage the evolution of cellular damage in human stroke. In 19 patients with ischemic stroke of presumed embolic or non-embolic cause we carried out diffusion-weighted and T2-weighted MR imaging within 48 h of onset, and obtained apparent diffusion coefficient of water (ADCw), and T2 weighted images. We used the signatures obtained from these ADCw/T2 maps to formulate two patterns of damage signifying accelerated or non-accelerated progression of cellular death after stroke onset. Those patients with the accelerated pattern corresponded to those with the neuroradiological (NRC) and clinical diagnosis (TOAST.1 and TOAST.2) of presumed embolic stroke, with clinical diagnosis performed blinded both to NRC and to SM. Agreement between the SM and NRC was substantial (kappa=0.62), moderate (0.60<kappa<0.40) between the SM or NRC and TOAST.2, and fair (0.40<kappa<0.20) among the SM or NRC and TOAST.1. We believe these results constitute a preliminary validation of the MR tissue signature modeling in clinical stroke assessment.

Adult↗

PubMed1996

Low pulsatility signals through the orbits.

BACKGROUND AND PURPOSE: Low pulsatility signals (LPS) on transcranial Doppler ultrasonography are detected (1) with arteriovenous malformations, (2) distal to hemodynamically significant stenosis, and (3) in venous structures. We describe focal LPS in the territory of the internal carotid artery siphon that do not represent any of the above conditions. METHODS: We performed retrospective and prospective reviews of transcranial Doppler studies on 3225 patients over 5 years. Clinical and radiological data of all patients with focal LPS were extracted. LPS was defined as a focal signal identified through the orbital windows with a low pulsatility index (< 0.6). RESULTS: Sixteen LPS (mean flow velocity [mean +/- SD], 62 +/- 11 cm/s; pulsatility index [mean +/- SD], 0.41 +/- 0.08; depth range, 46 to 72 mm) from 15 patients (mean +/- SD age, 45 +/- 15 years; 4 men, 11 women) were identified. LPS flow direction was away from the probe in 13 cases and toward it in 3. Presenting symptoms included headache, focal neurological deficits, dizziness, and pulsatile tinnitus. All patients had cranial MRI (MRI and MR angiography in 11). Three patients underwent conventional cerebral angiography. Arteriovenous malformations or significant arterial stenoses were not detected on any study. CONCLUSIONS: A focal signal from the internal carotid artery siphon region with low pulsatility index and normal mean flow velocity, identified in the absence of other transcranial Doppler abnormalities, is not related to an arteriovenous malformation or proximal arterial stenosis. LPS, as defined, are not of venous origin since mean flow velocity was in the arterial range. LPS are likely related to prominent venous flow in the cavernous sinus secondary to unusually strong pulsation of the intracavernous internal carotid artery.

Blood Flow Velocity↗