Multivariate Prognostic Model of Acute Stroke Combining Admission Infarct Location and Symptom Severity: A Proof-of-Concept Study.

BACKGROUND: The information on topographic distribution of acute ischemic infarct can contribute to prediction of functional outcome. We aimed to develop a multivariate model for stroke prognostication, combining admission clinical and imaging variables, including the infarct topology. METHODS: Acute ischemic stroke patients without baseline functional disability who had magnetic resonance imaging within 24 hours of onset or last-seen-well were included. The admission stroke severity was determined using the National Institutes of Health Stroke Scale (NIHSS) score. The relation between infarct location and outcome was assessed using both voxel-based and visual atlas-based analyses. The disability/death was defined by a modified Rankin Scale score greater than 2 at 3-month follow-up. RESULTS: Among 198 patients included in this study, higher admission NIHSS score (P < .001), larger infarct volume (P < .001), and major arterial occlusions (P < .001) were associated with disability/death in univariate analyses. On voxel-based analysis, infarcts in the middle centrum semiovale, insula, and midbrain/pons were associated with higher rates of disability/death. In multivariate analysis, admission NIHSS score (P < .001), infarction of insula (P = .005), and midbrain/pons (P = .006) were independent predictors of disability/death. In receiver operating characteristics analysis, a simple 0-to-3 scoring system using these 3 variables had an area under the curve of .812 for prediction of disability/death (P < .001). CONCLUSIONS: Admission symptom severity, infarction of insula, and midbrain/pons were independent predictors of clinical outcome in acute ischemic stroke patients. The methodology of this hypothesis-generating study can help conceive quantitative population-based probabilistic models for prognostication or treatment triage in stroke patients, combining admission clinical and imaging findings-including infarct topography.

Imaging features of neurotoxoplasmosis: A multiparametric approach, with emphasis on susceptibility-weighted imaging.

BACKGROUND: Neurotoxoplasmosis is a common opportunistic infection in HIV/AIDS patients. Imaging identification of neurotoxoplasmosis assists in timely treatment. PURPOSE: To delineate the frequency of imaging abnormalities in patients with neurotoxoplasmosis on different MR sequences with a particular focus on SWI, and NCCT. MATERIAL AND METHODS: The PACS database was retroactively searched over a 5-year period for patients with neurotoxoplasmosis who underwent MRI with SWI. Included patients had imaging features of neurotoxoplasmosis based on consensus review by two neuroradiologists, a clinical diagnosis of neurotoxoplasmosis at the time of MRI, and diagnostic confirmation based on positive serum or CSF serology or histopathology; 15 patients were included. The number of abnormal foci with restricted diffusion, increased FLAIR signal, intrinsic T1 hyperintensity, abnormal enhancement (CE-T1WI), and intrinsic hyperdensity on CT were recorded. RESULTS: Intralesional susceptibility signal (ISS) foci on SWI were observed in 93.3% of patients with neurotoxoplasmosis (mean size 5.2 ±â€¯3.8 mm). The average number of ISS foci was 3.9 per patient; 3/15 (20.0%) had a single ISS. Amongst other MR sequences, hyperintense FLAIR foci were the most common abnormalities observed (12.4 lesions/patient), followed by enhancing foci (8.2 lesions/patient), foci of restricted diffusion (7.1 lesions/patient), and intrinsic T1 hyperintense foci (3.4 lesions/patient). Abnormalities were least frequently observed on NCCT: abnormalities were identified in 5/15 (33.3%) patients, at a rate of 0.4 lesions/patient. CONCLUSION: ISS foci are present in the vast majority of neurotoxoplasmosis patients, likely representing hemorrhage. The incidence and frequency of other abnormal foci are highest on FLAIR, and lowest on NCCT.

Utility of coronal contrast-enhanced fat-suppressed FLAIR in the evaluation of optic neuropathy and atrophy.

BACKGROUND AND PURPOSE: Evaluating chronic sequelae of optic neuritis, such as optic neuropathy with or without optic nerve atrophy, can be challenging on whole brain MRI. This study evaluated the utility of dedicated coronal contrast-enhanced fat-suppressed FLAIR (CE-FS-FLAIR) MR imaging to detect optic neuropathy and optic nerve atrophy. MATERIALS AND METHODS: Over 4.5 years, a 3 mm coronal CE-FS-FLAIR sequence at 1.5T was added to the routine brain MRIs of 124 consecutive patients, 102 of whom had suspected or known demyelinating disease. Retrospective record reviews confirmed that 28 of these 102 had documented onset of optic neuritis >4 weeks prior to the brain MRI. These 28 were compared to the other 22 ("controls") of the 124 patients who lacked a history of demyelinating disease or visual symptoms. Using coronal CE-FS-FLAIR, two neuroradiologists separately graded each optic nerve (n = 50 patients, 100 total nerves) as either negative, equivocal, or positive for optic neuropathy or atrophy. The scoring was later repeated. RESULTS: The mean time from acute optic neuritis onset to MRI was 4.1 ± 4.6 years (range 34 days-17.4 years). Per individual nerve grading, the range of sensitivity, specificity, and accuracy of coronal CE-FS-FLAIR in detecting optic neuropathy was 71.4-77.1%, 93.8-95.4%, and 85.5-89.0%, respectively, with strong interobserver (k = 0.667 - 0.678, p < 0.0001), and intraobserver (k = 0.706 - 0.763, p < 0.0001) agreement. For optic atrophy, interobserver agreement was moderate (k = 0.437 - 0.484, p < 0.0001), while intraobserver agreement was moderate-strong (k = 0.491 - 0.596, p < 0.0001). CONCLUSION: Coronal CE-FS-FLAIR is quite specific in detecting optic neuropathy years after the onset of acute optic neuritis, but is less useful in detecting optic nerve atrophy.

Magnetization transfer and adiabatic R 1ρ MRI in the brainstem of Parkinson's disease.

BACKGROUND: In addition to classic midbrain pathology, Parkinson's disease (PD) is accompanied by changes in pontine and medullary brainstem structures. These additional abnormalities may underlie non-motor features as well as play a role in motor disability. METHODS: Using novel magnetic resonance imaging (MRI) methods based on rotating frame adiabatic R(1ρ) (i.e., measurements of longitudinal relaxation during adiabatic full passage pulses) and modified magnetization transfer (MT) MRI mapping, we sought to identify brainstem alterations in nine individuals with mild-moderate PD (off medication) and ten age-matched controls at 4 T. RESULTS: We discovered significant differences in MRI parameters between midbrain and medullary brainstem structures in control subjects as compared to PD patients. CONCLUSIONS: These findings support the presence of underlying functional/structural brainstem changes in mild-moderate PD.