Riikka Tulamo

Dr. Riikka Tulamo

orcid

Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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17 January 2012 in Acta Neuropathologica
Verified
Journal Article
Closed access
PDF file
JFJuhana Frösen
Juhana Frösen
RTRiikka Tulamo
Riikka Tulamo
APAnders Paetau
Anders Paetau
ELElisa Laaksamo
Elisa Laaksamo
MKMiikka Korja
Miikka Korja
JHJuha Hernesniemi
Juha Hernesniemi

12 March 2010 in Journal of NeuroInterventional Surgery
Verified
Journal Article
Closed access
PDF file
RTRiikka Tulamo
Riikka Tulamo
JFJuhana Frösen
Juhana Frösen
JHJuha Hernesniemi
Juha Hernesniemi
MNMika Niemelä
Mika Niemelä
Rupture of a saccular intracranial artery aneurysm (IA) causes subarachnoid hemorrhage, a significant cause of stroke and death. The current treatment options, endovascular coiling and clipping, are invasive and somewhat risky. Since only some IAs rupture, those IAs at risk for rupture should be identified. However, to improve the imaging of rupture-prone IAs and improve IA treatment, IA wall pathobiology requires more thorough knowledge. Chronic inflammation has become understood as an important phenomenon in IA wall pathobiology, featuring inflammatory cell infiltration as well as proliferative and fibrotic remodulatory responses. We review the literature on what is known about inflammation in the IA wall and also review the probable mechanisms of how inflammation would result in the degenerative changes that ultimately lead to IA wall rupture. We also discuss current options in imaging inflammation and how knowledge of inflammation in IA walls may improve IA treatment.

29 September 2016 in American Journal of Neuroradiology
Verified
Journal Article
Open access
PDF file
JCJ. Cebral
J. Cebral
EOE. Ollikainen
E. Ollikainen
BCB.J. Chung
B.J. Chung
FMF. Mut
F. Mut
VSV. Sippola
V. Sippola
JFJ. Frösen
J. Frösen
BACKGROUND AND PURPOSE: Saccular intracranial aneurysm is a common disease that may cause devastating intracranial hemorrhage. Hemodynamics, wall remodeling, and wall inflammation have been associated with saccular intracranial aneurysm rupture. We investigated how saccular intracranial aneurysm hemodynamics is associated with wall remodeling and inflammation of the saccular intracranial aneurysm wall. MATERIALS AND METHODS: Tissue samples resected during a saccular intracranial aneurysm operation (11 unruptured, 9 ruptured) were studied with histology and immunohistochemistry. Patient-specific computational models of hemodynamics were created from preoperative CT angiographies. RESULTS: More stable and less complex flows were associated with thick, hyperplastic saccular intracranial aneurysm walls, while slower flows with more diffuse inflow were associated with degenerated and decellularized saccular intracranial aneurysm walls. Wall degeneration (P = .041) and rupture were associated with increased inflammation (CD45+, P = .031). High wall shear stress (P = .018), higher vorticity (P = .046), higher viscous dissipation (P = .046), and high shear rate (P = .046) were associated with increased inflammation. Inflammation was also associated with lack of an intact endothelium (P = .034) and the presence of organized luminal thrombosis (P = .018), though overall organized thrombosis was associated with low minimum wall shear stress (P = .034) and not with the flow conditions associated with inflammation. CONCLUSIONS: Flow conditions in the saccular intracranial aneurysm are associated with wall remodeling. Inflammation, which is associated with degenerative wall remodeling and rupture, is related to high flow activity, including elevated wall shear stress. Endothelial injury may be a mechanism by which flow induces inflammation in the saccular intracranial aneurysm wall. Hemodynamic simulations might prove useful in identifying saccular intracranial aneurysms at risk of developing inflammation, a potential biomarker for rupture.

1 November 2006 in Neurosurgery
Verified
Journal Article
Closed access
PDF file
RTRiikka Tulamo
Riikka Tulamo
JFJuhana Frösen
Juhana Frösen
SJSami Junnikkala
Sami Junnikkala
APAnders Paetau
Anders Paetau
JPJanne Pitkäniemi
Janne Pitkäniemi
SMSeppo K Meri
Seppo K Meri
OBJECTIVE. Saccular cerebral artery aneurysm (SCAA) wall degeneration and inflammatory cell infiltrations associate with aneurysm rupture and subarachn

23 July 2018 in Journal of NeuroInterventional Surgery
Verified
Journal Article
Closed access
PDF file
RTRiikka Tulamo
Riikka Tulamo
JFJuhana Frösen
Juhana Frösen
JHJuha Hernesniemi
Juha Hernesniemi
MNMika Niemelä
Mika Niemelä
Rupture of a saccular intracranial artery aneurysm (IA) causes subarachnoid hemorrhage, a significant cause of stroke and death. The current treatment options, endovascular coiling and clipping, are invasive and somewhat risky. Since only some IAs rupture, those IAs at risk for rupture should be identified. However, to improve the imaging of rupture-prone IAs and improve IA treatment, IA wall pathobiology requires more thorough knowledge. Chronic inflammation has become understood as an important phenomenon in IA wall pathobiology, featuring inflammatory cell infiltration as well as proliferative and fibrotic remodulatory responses. We review the literature on what is known about inflammation in the IA wall and also review the probable mechanisms of how inflammation would result in the degenerative changes that ultimately lead to IA wall rupture. We also discuss current options in imaging inflammation and how knowledge of inflammation in IA walls may improve IA treatment.

1 June 2011 in Neurosurgery
Verified
Journal Article
Closed access
PDF file
MKMitja I Kurki
Mitja I Kurki
SHSanna-Kaisa Häkkinen
Sanna-Kaisa Häkkinen
JFJuhana Frösen
Juhana Frösen
RTRiikka Tulamo
Riikka Tulamo
MFMikael von Und zu Fraunberg
Mikael von Und zu Fraunberg
Seppo Ylä-HerttualaSeppo Ylä-Herttuala
Seppo Ylä-Herttuala
BACKGROUND:. Aneurysmal subarachnoid hemorrhage, almost always from saccular intracranial aneurysm (sIA), is a devastating form of stroke that affects t