Related Experiment Video
Updated: May 12, 2026
15:26
3D Modeling of the Lateral Ventricles and Histological Characterization of Periventricular Tissue in Humans and Mouse
Published on: May 19, 2015
14.1K
Change in Enlarged Perivascular Spaces over Time and Associations with Outcomes After Traumatic Brain Injury
Alexa E Walter1, Krupa Savalia2, Jason Yoon3
1Department of Neurology, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
Neurotrauma Reports
|August 15, 2024
Summary
Enlarged perivascular spaces (EPVs) after traumatic brain injury (TBI) did not change significantly over six months. Higher EPV counts at two weeks correlated with poorer functional recovery in TBI patients.
Area of Science:
- Neurology
- Radiology
- Neuroimaging
Background:
- Enlarged perivascular spaces (EPVs) are observable on MRI in neurological conditions, including traumatic brain injury (TBI).
- While EPVs are linked to cognitive and sleep issues, their clinical importance post-TBI is not fully understood.
- Understanding EPV dynamics and their association with outcomes is crucial for TBI management.
Purpose of the Study:
- To quantify the burden of EPVs over time using MRI following TBI.
- To investigate the relationship between EPV burden and post-TBI outcomes, including functional recovery and sleep disturbances.
- To explore EPVs as potential imaging biomarkers in TBI.
Main Methods:
- Thirty-two TBI participants underwent MRI and blood collection at 2 weeks and 6 months post-injury.
- EPV burden was assessed on T1 and FLAIR MRI sequences.
- Serum neurofilament light (NfL) and glial fibrillary acidic protein (GFAP) levels were measured; sleep and functional outcomes were evaluated.
Main Results:
- The total count of EPVs remained stable between 2 weeks and 6 months post-TBI.
- No significant association was found between EPV count and self-reported insomnia or sleep quality.
- A higher number of EPVs at 2 weeks post-TBI was significantly associated with incomplete functional recovery at 6 months.
Conclusions:
- EPV burden shows minimal change in the six months following TBI, suggesting they may represent stable structural findings.
- EPV count at two weeks post-TBI may serve as an early indicator of long-term functional recovery.
- Further research is needed to clarify the role of EPVs in TBI pathophysiology and their potential as prognostic imaging biomarkers.
Keywords:
enlarged perivascular spacesmagnetic resonance imagingperivascular spacestraumatic brain injuryMore Related Videos
Related Concept Videos
01:29Hemorrhagic Stroke ll: Pathophysiology
A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
01:26Bacterial Meningitis II: Pathophysiology
Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
01:14Increased Intracranial Pressure l: Introduction
Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
01:29Increased Intracranial Pressure ll: Pathophysiology
Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
01:19Cerebral Edema l: Introduction
Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
01:22Cerebral Edema ll: Pathophysiology
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...