Angelos Katramados
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Angelos Katramados has a total of 18 co-authors. Here are the top co-authors by number of shared publications:
- A.Y. Mohamud
Department of Neurology, Henry Ford Hospital, Detroit, MI, United States
1 shared publication - Ahmad Riad Ramadan
Henry Ford Hospital
1 shared publication - Alex Bou Chebl
Department of Neurology, Henry Ford Health System
1 shared publication - Brent Griffith
Henry Ford Health System
1 shared publication - Dawn Scozzari
Department of Neurology, Henry Ford Hospital, Detroit, MI, USA
1 shared publication Ghada Mohamed
Department of Neurology, Henry Ford Hospital, Detroit, MI, United States
1 shared publication
Latest Publications
- 4 March 2022
- Published by Elsevier in Clinical Neurology and Neurosurgery
- Vol. 215, 107199
Rituximab for prevention of strokes in cerebral rheumatoid vasculitis
- 4 March 2022
- Published by Elsevier in Clinical Neurology and Neurosurgery
- Vol. 215, 107199
Rituximab for prevention of strokes in cerebral rheumatoid vasculitis
- 1 June 2021
- Published by Elsevier in Journal of Stroke and Cerebrovascular Diseases
- Vol. 30 (6) , 105746
Impact of the COVID-19 Pandemic on Acute Stroke Care, Time Metrics, Outcomes, and Racial Disparities in a Southeast Michigan Health System
- 1 June 2021
- Published by Elsevier in Journal of Stroke and Cerebrovascular Diseases
- Vol. 30 (6) , 105746
Impact of the COVID-19 Pandemic on Acute Stroke Care, Time Metrics, Outcomes, and Racial Disparities in a Southeast Michigan Health System
- Open Access
- 3 May 2018
- Published by American Society of Neuroradiology (ASNR) in American Journal of Neuroradiology
- Vol. 39 (6) , 1185-1190
CSF Pressure Change in Relation to Opening Pressure and CSF Volume Removed
BACKGROUND AND PURPOSE: Idiopathic intracranial hypertension is a complex neurologic disorder resulting from increased intracranial pressure. Our aim was to determine whether a correlation exists between the CSF pressure-volume relationship, specifically the craniospinal elastance and pressure-volume index, in patients with idiopathic intracranial hypertension and whether opening pressure affects this relationship. MATERIALS AND METHODS: Lumbar punctures performed for suspected idiopathic intracranial hypertension from 2006 to 2017 were identified. Opening and closing pressures, CSF volume removed, and clinical diagnosis of idiopathic intracranial hypertension were obtained from the medical records. The craniospinal elastance (pressure change per milliliter of CSF removed) and pressure-volume index were calculated, and the Pearson correlation coefficients between both the craniospinal elastance and pressure-volume index and opening pressure were determined. Linear regression models of craniospinal elastance and the pressure-volume index and interaction terms with opening pressure were assessed for covariate influence on this association. RESULTS: One hundred sixteen patients were included in the final analysis. The mean craniospinal elastance according to opening pressure group was 0.52 ± 0.18 for 2O, 0.57 ± 0.20 for 20–29 cm H2O, 0.91 ± 0.28 for 30–39 cm H2O, and 1.20 ± 0.25 for ≥40 cm H2O. There was a positive linear association between opening pressure and craniospinal elastance with a 0.28 cm H2O/mL increase in craniospinal elastance (standard error = 0.03, P < .001) for every 10 cm H2O increase in opening pressure. Of the covariables analyzed, only age older than 50 years and total volume of CSF removed affected this association. CONCLUSIONS: As opening pressure increases, the craniospinal elastance increases in a linear fashion while the pressure-volume index decreases. Further studies are needed to determine whether these changes relate to the underlying pathophysiology of idiopathic intracranial hypertension or simply represent established CSF volume pressure dynamics.
- 3 May 2018
- Published by American Society of Neuroradiology (ASNR) in American Journal of Neuroradiology
- Vol. 39 (6) , 1185-1190
Open AccessCSF Pressure Change in Relation to Opening Pressure and CSF Volume Removed
BACKGROUND AND PURPOSE: Idiopathic intracranial hypertension is a complex neurologic disorder resulting from increased intracranial pressure. Our aim was to determine whether a correlation exists between the CSF pressure-volume relationship, specifically the craniospinal elastance and pressure-volume index, in patients with idiopathic intracranial hypertension and whether opening pressure affects this relationship. MATERIALS AND METHODS: Lumbar punctures performed for suspected idiopathic intracranial hypertension from 2006 to 2017 were identified. Opening and closing pressures, CSF volume removed, and clinical diagnosis of idiopathic intracranial hypertension were obtained from the medical records. The craniospinal elastance (pressure change per milliliter of CSF removed) and pressure-volume index were calculated, and the Pearson correlation coefficients between both the craniospinal elastance and pressure-volume index and opening pressure were determined. Linear regression models of craniospinal elastance and the pressure-volume index and interaction terms with opening pressure were assessed for covariate influence on this association. RESULTS: One hundred sixteen patients were included in the final analysis. The mean craniospinal elastance according to opening pressure group was 0.52 ± 0.18 for 2O, 0.57 ± 0.20 for 20–29 cm H2O, 0.91 ± 0.28 for 30–39 cm H2O, and 1.20 ± 0.25 for ≥40 cm H2O. There was a positive linear association between opening pressure and craniospinal elastance with a 0.28 cm H2O/mL increase in craniospinal elastance (standard error = 0.03, P < .001) for every 10 cm H2O increase in opening pressure. Of the covariables analyzed, only age older than 50 years and total volume of CSF removed affected this association. CONCLUSIONS: As opening pressure increases, the craniospinal elastance increases in a linear fashion while the pressure-volume index decreases. Further studies are needed to determine whether these changes relate to the underlying pathophysiology of idiopathic intracranial hypertension or simply represent established CSF volume pressure dynamics.