Hyperechogenicity of the thalamus and basal ganglia in very preterm infants

ISRCTN	ISRCTN25932453
DOI	https://doi.org/10.1186/ISRCTN25932453
Secondary identifying numbers	NL617, NTR676

Submission date: 29/06/2006
Registration date: 29/06/2006
Last edited: 08/01/2021

Recruitment status: No longer recruiting
Overall study status: Completed
Condition category: Nervous System Diseases

Prospectively registered

Protocol

Statistical analysis plan

Results

Individual participant data

Plain English summary of protocol

Not provided at time of registration

Contact information

Ms Lara Leijser
Scientific

Leiden University Medical Center (LUMC)
Willem-Alexander Kinder- en Jeugdcentrum
Postzone J6-S
P.O. Box 9600
Leiden
2300 RC
Netherlands

Phone	+31 (0)71 5262909
Email	L.M.Leijser@lumc.nl

Study information

Study design	Non-randomized, single centre, parallel group study
Primary study design	Observational
Secondary study design	Cohort study
Study setting(s)	Hospital
Study type	Other
Scientific title	Hyperechogenicity of the thalamus and basal ganglia in very preterm infants
Study objectives	The principal aim of this research project is to establish the origin of increased echogenicity in the thalamus and basal ganglia (TBG), an ultrasonographic finding frequently encountered in very preterm infants. It is not known whether echodensities (ED) of TBG is a normal maturational phenomenon or a pathological process with consequences for neurological development. ED/TBG may, like transient ED in the frontal white matter, represent normal maturational changes occurring in the thalamus, basal ganglia, and/or the surrounding brain tissue. However, it may also represent damage to the developing brain, like more inhomogeneous ED in TBG in (near) term infants, unilateral or localized ED in TBG in preterm infants, linear and/or punctate ED in TBG in preterm and full term infants, and long-lasting ED in the periventricular white matter in preterm infants do. If so, ED/TBG is an important finding and may be associated with an unfavourable or even poor neurological prognosis. We want to explore whether ED/TBG is a pathological phenomenon or a normal (maturational) phenomenon occurring in the immature brain, and to establish the possible consequences of ED/TBG for short and long term neurological outcome of very preterm infants.
Ethics approval(s)	Not provided at time of registration
Health condition(s) or problem(s) studied	Preterm infants with hyperechogenicity of TBG
Intervention	In all very preterm infants born after a gestational age of less than 32 weeks, serial cerebral ultrasonography (CUS) examinations will be performed according to the standard protocol. All CUS examinations will be evaluated for the presence of diffuse ED/TBG. This will result in a division of all preterm infants into two groups, i.e. a group of preterm infants with ED/TBG and a group of preterm infants without ED/TBG. All infants (infants with and without ED/TBG) will undergo a single cerebral magnetic resonance imaging (MRI) examination around term date. In addition, they will visit our follow-up clinic around term date and at corrected ages of 12 and 24 months, when their neurodevelopment will be assessed. The results obtained from CUS, MRI and follow-up will be compared between the infants with ED/TBG and the infants without ED/TBG. The only difference between the two groups of infants is that in one group ED/TBG is detected on CUS, whereas in the other group ED/TBG is not detected. There is no difference between groups in the number of examinations.
Intervention type	Other
Primary outcome measure	The origin and clinical significance of ED/TBG in very preterm infants
Secondary outcome measures	Improvement in the prediction of neurological prognosis of individual preterm infants and the understanding of maturational and pathological processes in the preterm brain
Overall study start date	03/04/2006
Completion date	31/03/2010

Eligibility

Participant type(s)	Patient
Age group	Child
Sex	Both
Target number of participants	140
Total final enrolment	130
Key inclusion criteria	Infants born after a gestational age of less than 32 weeks in the Leiden University Medical Center between May 2006 - August 2007.
Key exclusion criteria	Congenital anomalies or serious acquired abnormalities of the central nervous system, chromosomal disorders, metabolic disorders, neonatal meningitis or sepsis.
Date of first enrolment	03/04/2006
Date of final enrolment	31/03/2010

Locations

Countries of recruitment

Netherlands

Study participating centre

Leiden University Medical Center (LUMC)

Leiden
2300 RC
Netherlands

Sponsor information

Leiden University Medical Center (LUMC) (The Netherlands)
University/education

P.O. Box 9600
Leiden
2300 RC
Netherlands

"ROR"	https://ror.org/05xvt9f17

Funders

Funder type

University/education

Leiden University Medical Center (LUMC)

No information available

ZonMw (The Netherlands Organization for Health Research and Development)
Private sector organisation / Other non-profit organizations

Alternative name(s): Netherlands Organisation for Health Research and Development
Location: Netherlands

Results and Publications

Intention to publish date
Individual participant data (IPD) Intention to share	No
IPD sharing plan summary	Not provided at time of registration
Publication and dissemination plan	Not provided at time of registration
IPD sharing plan

Study outputs

Output type	Details	Date created	Date added	Peer reviewed?	Patient-facing?
Results article	results	01/03/2011	08/01/2021	Yes	No

Editorial Notes

08/01/2021: The following changes have been made:
1. Publication reference added.
2. The final enrolment number has been added from the reference.
3. The NTR numbers have been added.