Hyperechogenicity of the thalamus and basal ganglia in very preterm infants
| ISRCTN | ISRCTN25932453 |
|---|---|
| DOI | https://doi.org/10.1186/ISRCTN25932453 |
| Protocol serial number | NL617, NTR676 |
| Sponsor | Leiden University Medical Center (LUMC) (The Netherlands) |
| Funders | Leiden University Medical Center (LUMC), ZonMw (The Netherlands Organization for Health Research and Development) |
- 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
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 |
|---|---|
| L.M.Leijser@lumc.nl |
Study information
| Primary study design | Observational |
|---|---|
| Study design | Non-randomized, single centre, parallel group study |
| Secondary study design | Cohort study |
| 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(s) |
The origin and clinical significance of ED/TBG in very preterm infants |
| Key secondary outcome measure(s) |
Improvement in the prediction of neurological prognosis of individual preterm infants and the understanding of maturational and pathological processes in the preterm brain |
| Completion date | 31/03/2010 |
Eligibility
| Participant type(s) | Patient |
|---|---|
| Age group | Child |
| Sex | All |
| Target sample size at registration | 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
2300 RC
Netherlands
Results and Publications
| Individual participant data (IPD) Intention to share | No |
|---|---|
| IPD sharing plan summary | 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.
