Petra Klinge

Dr. Petra Klinge

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Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

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

Representative Publications

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1 January 2014 in Fluids and Barriers of the CNS
Verified
Journal Article
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TBThomas Brinker
Thomas Brinker
ESEdward Stopa
Edward Stopa
JMJohn Morrison
John Morrison
Petra KlingePetra Klinge
Petra Klinge
According to the traditional understanding of cerebrospinal fluid (CSF) physiology, the majority of CSF is produced by the choroid plexus, circulates through the ventricles, the cisterns, and the subarachnoid space to be absorbed into the blood by the arachnoid villi. This review surveys key developments leading to the traditional concept. Challenging this concept are novel insights utilizing molecular and cellular biology as well as neuroimaging, which indicate that CSF physiology may be much more complex than previously believed. The CSF circulation comprises not only a directed flow of CSF, but in addition a pulsatile to and fro movement throughout the entire brain with local fluid exchange between blood, interstitial fluid, and CSF. Astrocytes, aquaporins, and other membrane transporters are key elements in brain water and CSF homeostasis. A continuous bidirectional fluid exchange at the blood brain barrier produces flow rates, which exceed the choroidal CSF production rate by far. The CSF circulation around blood vessels penetrating from the subarachnoid space into the Virchow Robin spaces provides both a drainage pathway for the clearance of waste molecules from the brain and a site for the interaction of the systemic immune system with that of the brain. Important physiological functions, for example the regeneration of the brain during sleep, may depend on CSF circulation.

16 May 2024 in Nature Reviews Disease Primers
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Journal Article
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Kristopher T. KahleKristopher T. Kahle
Kristopher T. Kahle
Petra KlingePetra Klinge
Petra Klinge
JKJenna E. Koschnitzky
Jenna E. Koschnitzky
AKAbhaya V. Kulkarni
Abhaya V. Kulkarni
NMNanna MacAulay
Nanna MacAulay
JSJennifer M. Strahle
Jennifer M. Strahle

1 April 2008 in Clinical Neurology and Neurosurgery
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Journal Article
Closed access
Petra KlingePetra Klinge
Petra Klinge
DBDavid Brooks
David Brooks
ASAmir Samii
Amir Samii
EWEva Weckesser
Eva Weckesser
JHJörg van Den Hoff
Jörg van Den Hoff
GBGeorg Berding
Georg Berding

1 July 2016 in Journal of Craniofacial Surgery
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Journal Article
Closed access
RIRajiv J. Bs Iyengar
Rajiv J. Bs Iyengar
Petra KlingePetra Klinge
Petra Klinge
WCWendy S. Chen
Wendy S. Chen
JBJerrold Boxerman
Jerrold Boxerman
SSStephen R. Sullivan
Stephen R. Sullivan
HTHelena O. Taylor
Helena O. Taylor
Background: The natural history of unrepaired craniosynostosis is not well defined. Delayed surgical intervention carries greater risk of postoperative complications and its functional benefits for older patients are poorly characterized. The authors reviewed patients in whom children presented beyond 1 year of age to better understand the natural history of craniosynostosis, and the risk–benefit relationship for delayed reconstruction. Methods: After institutional IRB approval the authors conducted a retrospective review of patients who presented after 1 year of age with craniosynostosis. Type of craniosynostosis, age at evaluation, medical history, surgical findings, developmental abnormalities, ophthalmologic findings, and clinical course were reviewed. Results: Ten patients with delayed presentation for craniosynostosis were identified. The mean age at presentation was 6.8 years ± 4.2 years (range, 3–17 years). Seven of 10 patients presented with developmental delay. Five patients presented with debilitating headaches. Five patients presented with comorbid Chiari malformations, 3 of whom required surgical decompression. Two patients had papilledema. Four patients underwent intracranial pressure monitoring, with elevated pressures found in 3 patients. Six patients underwent delayed cranial vault remodeling. There were no peri- or postoperative complications, including infection or residual bony defects, in those undergoing delayed operation. Conclusions: Children who present in a delayed fashion with unrepaired craniosynostosis have high rates of debilitating headaches, developmental delays, head shape anomalies, and Chiari malformation. Five patients reporting preoperative headaches noted subjective improvements in headaches following delayed operation. Cranial reconstruction can be safely performed at an older age and is appropriate to consider in carefully selected patients for aesthetic and/or functional concerns.

16 December 2008 in Fluids and Barriers of the CNS
Verified
Journal Article
Open access
PDF file
HJHazel C Jones
Hazel C Jones
Petra KlingePetra Klinge
Petra Klinge
Hydrocephalus 2008 was held 17–20 September in Hannover, Germany, at the invitation of Petra M Klinge (President), co-hosted by Joachim K. Krauss (Vice President), and Madjid Samii (Honorary President). This meeting was a successor to Hydrocephalus 2006 held in Göteborg, Sweden, organised by Past-President, Carsten Wikkelso. The conference began with a general introductory session of six talks including three invited lectures, followed by eighteen parallel sessions. Subjects covered were hydrocephalus signs, symptoms and diagnosis, especially in normal pressure hydrocephalus; cerebrospinal fluid (CSF) physics and dynamics; CSF function and modelling of function; dementia and quality of life, economy, health care and rehabilitation; neuropsychology, cognition and outcome assessment; neuroimaging, functional imaging and non-invasive diagnostics; paediatric and adolescent hydrocephalus; intelligent shunt and valve design (e.g. telemetry, adjustable and antimicrobial shunts); endoscopic third ventriculostomy; technical advances and image-guided surgical approaches in the treatment of hydrocephalus; brain metabolism, biomarkers and biophysics; co-morbidity, classification and aetiology; epidemiology, registries and clinical trials; experimental hydrocephalus; and pharmaceutical modulation of central nervous system function (CNS drug delivery). Each session began with introductory talks from the invited chairpersons followed by six to eight submitted oral presentations. Overall, 136 oral presentations and 18 posters were presented, the abstracts of which were published elsewhere 1. We present here an account of the introductory session, the invited chairperson's talks and the concluding remarks by Anthony Marmarou.

1 July 2021 in Journal of Neurosurgery: Spine
Verified
Journal Article
Closed access
PDF file
Petra KlingePetra Klinge
Petra Klinge
AMAbigail McElroy
Abigail McElroy
JDJohn E. Donahue
John E. Donahue
TBThomas Brinker
Thomas Brinker
ZGZiya L. Gokaslan
Ziya L. Gokaslan
MBMichael D. Beland
Michael D. Beland
OBJECTIVE: The craniocervical junction (CCJ) is anatomically complex and comprises multiple joints that allow for wide head and neck movements. The thecal sac must adjust to such movements. Accordingly, the thecal sac is not rigidly attached to the bony spinal canal but instead tethered by fibrous suspension ligaments, including myodural bridges (MDBs). The authors hypothesized that pathological spinal cord motion is due to the laxity of such suspension bands in patients with connective tissue disorders, e.g., hypermobile Ehlers-Danlos syndrome (EDS). METHODS: The ultrastructure of MDBs that were intraoperatively harvested from patients with Chiari malformation was investigated with transmission electron microscopy, and 8 patients with EDS were compared with 8 patients without EDS. MRI was used to exclude patients with EDS and craniocervical instability (CCI). Real-time ultrasound was used to compare the spinal cord at C1–2 of 20 patients with EDS with those of 18 healthy control participants. RESULTS: The ultrastructural damage of the collagen fibrils of the MDBs was distinct in patients with EDS, indicating a pathological mechanical laxity. In patients with EDS, ultrasound revealed increased cardiac pulsatory motion and irregular displacement of the spinal cord during head movements. CONCLUSIONS: Laxity of spinal cord suspension ligaments and the associated spinal cord motion disorder are possible pathogenic factors for chronic neck pain and headache in patients with EDS but without radiologically proven CCI.