American Journal of Neuroradiology 25:289-290, February 2004
© 2004 American Society of Neuroradiology
Case Report
BRAIN
Infarction of the Choroid Plexus
David S. Liebeskinda and
Robert W. Hursta
a From the Departments of Neurology and Radiology, University of Pennsylvania, Philadelphia, PA
Address correspondence to David S. Liebeskind, MD, Comprehensive Stroke Center and Department of Neurology, University of Pennsylvania, 3 West Gates Building, 3400 Spruce Street, Philadelphia, PA 19104-4283
 |
Abstract
|
|---|
Summary: Infarction of the choroid plexus may result from ischemia
in the distribution of the medial posterior choroidal artery.
Diffusion-weighted imaging may depict this unusual stroke syndrome.
The clinical and radiologic aspects of this rare condition are
discussed taking into consideration the anatomy and pathophysiology
of the choroid plexus.
|
Introduction
|
|---|
The choroid plexus plays a pivotal role in the regulation of
CSF, determining permeability of the blood-CSF barrier, containing
various types of receptors, and secreting numerous growth and
trophic factors (
1). Despite the elaborate function of the choroid
plexus, pathologic derangements of this structure are of rare
clinical significance. Diffusion-weighted (DW) imaging may reveal
clinically silent lesions of the choroid plexus. We describe
an unusual case of infarction of the choroid plexus due to medial
posterior choroidal artery stroke.
|
Case Report
|
|---|
A 54-year-old man with hyperparathyroidism presented with acute-onset
right hemisensory loss and hemiparesis without visual impairment.
After 30 minutes, these symptoms resolved with the exception
of minimal right face and hand numbness. Two days later, he
had abrupt-onset, complete right hemisensory loss. On hospital
admission, noncontrast CT revealed a hypoattenuated lesion consistent
with a subacute left thalamocapsular lacunar stroke. Fluctuations
in the severity of his hemisensory deficits correlated with
blood pressure readings over a period of several days, without
associated neurologic deficits. DW imaging performed 5 days
after the initial onset of symptoms illustrated thalamocapsular
lacunar infarction due to thalamogeniculate ischemia, a splenial
lesion due to pericallosal involvement, and limited infarction
of the occipital cortex due to distal posterior cerebral artery
involvement (
Fig 1). Infarction of the choroid plexus in the
left lateral ventricle was also demonstrated on DW images (
Fig 2).
Apparent diffusion coefficient (ADC) maps confirmed restricted
diffusion in all involved regions, with only minimal reduction
of ADC values in the choroid plexus lesion (
Fig 3). MR angiography
demonstrated a segmental occlusion of the left posterior cerebral
artery that was corroborated with conventional angiography.
The presence of prominent vascular calcifications and mobile
aortic arch atheromata prompted further investigation with CT
angiography (CTA). CTA demonstrated in situ calcification of
the posterior cerebral artery (
Fig 4). After several days of
antiplatelet therapy and vigorous hydration, his clinical symptoms
subsided with only mild right hemisensory loss.
View larger version (92K):
[in this window]
[in a new window]
|
FIG 1. DW image reveals scattered hyperintensities in the vascular distribution of distal branches of the left posterior cerebral artery, including the superficial cortical branches, thalamogeniculate, and pericallosal arteries.
| |
View larger version (92K):
[in this window]
[in a new window]
|
FIG 3. ADC map shows only minimal reduction in coefficient values within the choroid plexus lesion (arrow).
| |
|
Discussion
|
|---|
To the best of our knowledge, infarction of the choroid plexus
has not been described previously. This unusual pattern of ischemia
likely resulted from involvement of a medial posterior choroidal
artery, emanating from the posterior cerebral artery in close
proximity to the thalamogeniculate perforators that caused the
thalamocapsular lacune (
2,
3). The scattered infarcts in the
distribution of various distal branches of the posterior cerebral
artery, including the medial posterior choroidal, may have developed
insidiously in association with progressive stenosis of the
parent vessel. Variability in the degree of the ADC decrements
may be due to differing ages of the ischemic lesions, although
interpretation of DW abnormalities of the choroid plexus may
be limited by inherent differences with respect to brain parenchyma.
The differential diagnosis of DW abnormalities in the intraventricular
space includes lesions of the choroid plexus, such as cysts
and xanthogranulomata, intraventicular hemorrhage, and pyogenic
ventriculitis. DW abnormalities of the choroid plexus may be
caused by a variety of choroid plexus cysts and xanthogranulomata,
although conventional MR imaging may help differentiate these
lesions on the basis of appearance and location. The DW abnormality
visualized in this case is located in an unusual location for
a cystic lesion, and xanthogranuloma typically has bilateral
involvement. Intraventricular hemorrhage and pyogenic ventriculitis
may produce DW abnormalities, although extension into adjacent
ventricular structures in dependent fashion and corresponding
signal intensity abnormalities at conventional MR imaging may
be expected. Such neuroimaging features were not observed in
this case, because the DW abnormality was restricted to a focal
region of the choroid plexus. The simultaneous depiction of
multifocal DW abnormalities in the distribution of sibling tributaries
of the posterior cerebral artery supports the diagnosis of choroidal
infarction.
Medial posterior choroidal infarcts are rare, with neurologic findings that may be difficult to discern from adjacent lesions (4). Because most posterior cerebral artery infarcts are embolic and associated with more proximal ischemia, involvement of the medial posterior choroidal artery may go unrecognized.
Anastomoses of the anterior and posterior choroidal arteries are believed to protect the highly vascular choroid plexus from ischemia. Despite the presumed luxuriant collateral circulation of the choroid plexus, recent investigations of focal cerebral ischemia and hypoxic-ischemic injury have demonstrated the relative vulnerability of this structure (5, 6). Apoptotic and necrotic cell loss in the choroid plexus may result from either hypoxic-ischemic injury or secondary involvement due to parenchymal ischemia (7). The choroid plexus of the lateral ventricle appears to be more vulnerable to ischemia compared with the portion of this structure residing in the fourth ventricle (8). Collateral blood flow to the choroid plexus likely also varies by the specific anatomic segment of this structure.
Localized infarction of the choroid plexus probably has a negligible effect on CSF regulation without any clinical manifestations. Alteration of the permeability of the blood-CSF barrier may theoretically exacerbate cerebral edema following stroke; however, stabilization of brain fluid balance may be rapidly restored by the choroid plexus (9). Although infarction of the choroid plexus may be clinically silent, recognition of this entity may expand the differential diagnosis of intraventricular lesions with characteristic features that may exclude clinically portentous diagnoses.
|
Conclusion
|
|---|
Increasingly routine use of DW image for stroke will likely
reveal various clinically silent infarct patterns that may invoke
an underlying stroke or vascular mechanism. Unusual stroke syndromes
such as medial posterior choroidal artery infarction may be
readily apparent on DW images, leading the clinician to search
for relatively subtle aspects of stroke origin. Choroidal infarction
as demonstrated by DW imaging may have limited clinical significance
yet may provide further insight into the pathophysiology of
this complex structure.
|
References
|
|---|
- Chodobski A, Szmydynger-Chodobska J. Choroid plexus: target for polypeptides and site of their synthesis.
Microsc Res Tech2001; 52
:65
–82[Medline]
- Wolfram-Gabel R, Maillot C, Koritke JG, Laude M. Vascularization of the tela choroidea of the 3rd ventricle in man [in French].
Arch Anat Histol Embryol1984; 67
:3
–42[Medline]
- Milisavljevic MM, Marinkovic SV, Gibo H, Puskas LF. The thalamogeniculate perforators of the posterior cerebral artery: the microsurgical anatomy.
Neurosurgery1991; 28
:523
–529[Medline]
- Neau JP, Bogousslavsky J. The syndrome of posterior choroidal artery territory infarction.
Ann Neurol1996; 39
:779
–788[Medline]
- Nagahiro S, Goto S, Korematsu K, et al. Disruption of the blood-cerebrospinal fluid barrier by transient cerebral ischemia.
Brain Res1994; 633
:305
–311[Medline]
- Rothstein RP, Levison SW. Damage to the choroid plexus, ependyma and subependyma as a consequence of perinatal hypoxia/ischemia.
Dev Neurosci2002; 24
:426
–436[Medline]
- Li Y, Chen J, Chopp M. Cell proliferation and differentiation from ependymal, subependymal and choroid plexus cells in response to stroke in rats.
J Neurol Sci2002; 193
:137
–146[Medline]
- Palm D, Knuckey N, Guglielmo M, et al. Choroid plexus electrolytes and ultrastructure following transient forebrain ischemia.
Am J Physiol1995; 269
:R73
–R79
- Johanson CE, Palm DE, Primiano MJ, et al. Choroid plexus recovery after transient forebrain ischemia: role of growth factors and other repair mechanisms.
Cell Mol Neurobiol2000; 20
:197
–216[Medline]
Received April 16, 2003;
accepted after revision May 20, 2003.
TOP
Abstract
Introduction