DOI:10.2214/AJR.04.1923
AJR 2006; 187:1048-1053
© American Roentgen Ray Society
Comparison of MRI Sequences to Detect Ventriculitis
Akira Fujikawa1,
Kazuhiro Tsuchiya2,
Keita Honya2 and
Toshiaki Nitatori2
1 Department of Radiology, Japan Self-Defense Forces Central Hospital, 1-2-24,
Ikejiri, Setagaya, Tokyo 154-8532, Japan.
2 Department of Radiology, Kyorin University Hospital School of Medicine, Tokyo,
Japan.
Received December 18, 2004;
accepted after revision August 22, 2005.
Address correspondence to A. Fujikawa.
Abstract
OBJECTIVE. The ability of different MRI sequences to depict
characteristic findings suggestive of ventriculitis was compared.
CONCLUSION. The study comprised 20 brain MRI studies in 13 patients
who had a final diagnosis of ventriculitis. Both diffusion-weighted imaging
and FLAIR imaging were equally and highly sensitive for detecting
intraventricular debris and pusthe most common MRI finding suggestive
of ventriculitis. FLAIR imaging was superior to contrast-enhanced T1-weighted
imaging for depicting ventricular wall abnormalitiesa less common
finding that also is suggestive of ventriculitis.
Keywords: brain diffusion-weighted imaging FLAIR imaging infectious diseases MRI
Introduction
Ventriculitis is an uncommon CNS infection that has been described using a
variety of terms including ependymitis, intraventricular abscess, ventricular
empyema, and pyocephalus [1].
This variety of terms reflects various facets of the disease's pathologic
process. Because ventriculitis is a severe intracranial infection that can
lead to serious sequelae and death, prompt diagnosis is necessary. However,
the clinical features of ventriculitis are often obscure and nonspecific. MRI
plays an important role as a first-line diagnostic tool in the diagnosis of
ventriculitis [2].
Previously reported characteristic MRI findings of ventriculitis include
intraventricular debris and pus, abnormal periventricular and subependymal
signal intensity, and enhancement of the ventricular lining on conventional
MRI sequences [3,
4]. In addition, a few reports
have illustrated the usefulness of diffusion-weighted imaging for detecting
intraventricular debris and pus
[1,
3,
5]. We have encountered cases
of ventriculitis in which the above MRI features were subtle on some MR pulse
sequences but obvious on others. Thus, knowing which MRI sequences are useful
for detecting the characteristic findings of ventriculitis is important for
daily clinical practice.
To the best of our knowledge, the utility of different MRI sequences for
detecting the characteristic findings of ventriculitis has not been compared.
In this study, we sought to determine which combinations of MRI sequences and
findings were useful for the diagnosis of ventriculitis.
Materials and Methods
By searching the computer database of our institution's department of
radiology, we identified 13 patients who had been treated between November
1999 and July 2004 and were strongly suspected of having ventriculitis based
on their MRI findings. The medical records of these patients were reviewed by
two of the authors to obtain clinical follow-up information including
laboratory, treatment, and outcome data and to confirm the final diagnosis
based on the radiologic and clinical findings. The diagnoses of the 13
patients were consistent with ventriculitis. The patients, eight males and
five females, had a mean age of 50.5 years (age range, newborn-85 years). The
pathogens detected were Klebsiella pneumoniae (n = 1),
Staphylococcus aureus (n = 1), Streptococcus
pneumoniae (n = 2), Enterobacter cloacae (n =
1), Enterobacter aerogenes (n = 1), Escherichia
coli (n = 1), Mycobacterium tuberculosis (n =
1), Pseudomonas aeruginosa (n = 2), Cryptococcus
neoformans (n = 1), and unknown (n = 2). The specimens
for cultures and Gram stains were obtained by lumbar puncture (n =
9), ventriculostomy tube (n = 3), and abscess drainage (n =
1). Three patients were clinically improved. Five patients had prolonged
disturbance of consciousness. Five patients died during the study's time
course (2-73 days after MRI). Underlying conditions of these patients included
myelodysplastic syndrome (n = 1), lymphocytic leukemia (n =
1), postclipping of cerebral aneurysm (n = 1), malignant lymphoma
(n = 1), pneumonia (n = 1), severe facial bone fracture
(n = 1), AIDS (n = 2), mastoiditis and petrositis
(n = 1), postresection of meningioma (n = 1), and cerebellar
abscess (n = 1). Two patients had no risk factor. A total of 20 brain
MRI studies performed in these 13 patients were included in the imaging
analyses.
All MRI was performed using one of three 1.5-T imaging systems (Visart or
Exelart, Toshiba Medical Systems; Gyroscan Intera, Philips Medical Systems).
All MRI studies were performed according to our institution's protocol for
brain infection and inflammation, although the imaging parameters varied
slightly depending on the manufacturer of the system. The MRI protocol
included axial fast spin-echo T2-weighted sequences (TR/TE range,
4,000-4,900/90-120; field of view [FOV], 18-22 x 22 cm; matrix, 160-192
x 256-384; number of excitations [NEX], 1-2; echo-train length, 13, 15,
or 17; receiver bandwidth, 39.68, 41.856, or 62.464 kHz); axial
contrast-enhanced spin-echo T1-weighted sequences (450-540/10-15; FOV, 18-22
x 22 cm; matrix, 160-176 x 258-384; NEX, 1-2); axial FLAIR
sequences (8,000-10,000/105-120; FOV, 18 x 22; matrix, 160-192 x
256-320; NEX, 1-2; inversion time, 2,300-2,600 msec); and axial single-shot
spin-echo echo-planar diffusion-weighted sequences with b values of 0 and
1,000 s/mm2 along all three orthogonal axes (4,000-8,000/95-120;
FOV, 22-25 x 26-30 cm; matrix, 128 x 128; NEX, 1). Calculated
apparent diffusion coefficient (ADC) maps were also obtained.
Three radiologists with experience in brain imaging retrospectively
reviewed a total of 100 hard-copy MR images. Hard-copy images of each sequence
were separated from each other and randomly mixed. Each radiologist
independently assessed the following findings: the presence of abnormal
intraventricular signal intensity, the presence of abnormal periventricular
signal intensity, and the presence of contrast enhancement of the ventricular
wall on contrast-enhanced T1-weighted images. The presence of other MRI
findings associated with intracranial inflammation, including hydrocephalus,
meningitis, brain abscess, cerebritis, and choroid plexitis, was also
assessed. Abnormal intensities on the diffusion-weighted images were
correlated with corresponding findings on the ADC maps. The ADC values of
abnormal intraventricular intensities and normal-appearing intraventricular
CSF were obtained by calculating the mean values of three circular regions of
interest (ROIs), each of which was 2-5 mm in diameter, on the ADC maps. For
abnormal periventricular intensities on FLAIR images, each reviewer attempted
to subjectively distinguish between the presence of an inflammatory process
and an age-related normal variant. Interpretation discrepancies were resolved
by the judgment of a third radiologist.
We followed our institution's ethical guidelines. At our institution,
institutional review board approval and informed consent are not required for
retrospective reviews of imaging studies and medical records.
Results
Of the 20 MRI studies, intraventricular abnormal intensities were present
in 19 (95%) of the diffusion-weighted images, 19 (95%) of the FLAIR images, 13
(65%) of the T2-weighted images, and 10 (50%) of the contrast-enhanced
T1-weighted images. Of all MRI studies, abnormal intensities were detected in
bilateral ventricles in 12 of the diffusion-weighted images, nine of the FLAIR
images, five of the T2-weighted images, and five of the contrast-enhanced
T1-weighted images. Abnormal intraventricular signal intensities relative to
the signal intensities for normal CSF were hyperintense on the
diffusion-weighted and FLAIR images, slightly hypointense on the T2-weighted
images, and slightly hyperintense on the contrast-enhanced T1-weighted images
(Figs. 1A,
1B,
1C,
1D, and
1E).

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Fig. 1A 68-year-old man with severe mastoiditis and acute petrositis.
T2-weighted image shows areas of slight hypointensity relative to CSF in
bilateral trigone of lateral ventricle. This finding is suggestive of
intraventricular debris and pus. Slight ventricular wall abnormality is
noted.
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Fig. 1B 68-year-old man with severe mastoiditis and acute petrositis.
FLAIR image shows hyperintense intraventricular lesions relative to CSF and
hyperintensity along ventricular lining, suggesting ependymitis.
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Fig. 1C 68-year-old man with severe mastoiditis and acute petrositis.
Contrast-enhanced T1-weighted image shows abnormal curvilinear enhancement
along the ventricular wall. Intraventricular debris and pus are slightly
hyperintense relative to CSF.
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Fig. 1D 68-year-old man with severe mastoiditis and acute petrositis.
Diffusion-weighted image shows areas of conspicuous intraventricular and
periventricular hyperintensity, indicating restricted water diffusion in those
areas.
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Fig. 1E 68-year-old man with severe mastoiditis and acute petrositis.
Apparent diffusion coefficient (ADC) map shows areas of decreased ADC values
in corresponding lesions on diffusion-weighted image (D).
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All abnormal intraventricular signal intensities were located in either the
occipital horn or the trigone of the lateral ventricle that is, in the
dependent portion of the lateral ventricleat the time of MRI. In
addition, in three studies performed in three patients, abnormal intensities
were seen in the fourth ventricle. In all patients, areas of intraventricular
hyperintensity on the diffusion-weighted images corresponded with decreased
ADC values. The ADC values of the intraventricular lesions ranged from 695
± 72 x 10-3 mm2/s to 1,180 ± 47
x 10-3 mm2/s (mean, 860 ± 68 x
10-3 mm2/s). These ADC values were significantly lower
than those of the intraventricular CSF, which ranged from 2,780 ± 563
x 10-3 mm2/s to 3,621 ± 822 x
10-3 mm2/s (mean, 3,008 ± 692 x
10-3 mm2/s).
Abnormal periventricular intensities were detected in 17 (85%) of the FLAIR
images, 11 (55%) of the diffusion-weighted images, and six (30%) of the
T2-weighted images. Asymmetric periventricular abnormalities were seen in 12
of the FLAIR images, 10 of the diffusion-weighted images, and five of the
T2-weighted images. Enhancement of the ventricular lining was observed in 12
(60%) of the 20 MRI studies. Asymmetric contrast enhancement of the
periventricular region was seen in 10 studies. In 11 (55%) of the 20 MRI
studies, hydrocephalus was observed in each of the sequences.
Specific MRI findings were found in association with a variety of
conditions, including meningitis (n = 13), cerebral abscess
(n = 2), cerebritis (n = 2), subdural empyema (n =
3), cerebellar abscess (n = 1), maxillary sinusitis (n = 2),
mastoiditis with otitis media (n = 1), brain contusion (n =
2), postoperative changes (n = 3), and suspected choroid plexitis
(n = 5).
Discussion
In our series, the most frequent sign of ventriculitis (95% both on
diffusion-weighted and FLAIR images) was intraventricular debris and pus.
Abnormal periventricular intensities or enhancements were observed less
frequently (85% on FLAIR images and 60% on contrast-enhanced T1-weighted
images). These results are in agreement with those of a previous study by
Fukui et al. [3]. The present
study showed that diffusion-weighted and FLAIR imaging concordantly showed
intraventricular debris and pus in the same patients with an equally high
detection rate. Thus, both of these sequences can be expected to contribute to
the diagnosis of ventriculitis. However, our impression is that
diffusion-weighted imaging is highly sensitive for detecting
ventriculitis.
The number of lesions detected in bilateral ventricles was higher on the
diffusion-weighted images than on the FLAIR images. This discrepancy was
likely caused by a difference in lesion conspicuity between the sequences.
Although a quantitative evaluation was not performed, hyperintense
intraventricular debris and pus were more conspicuous on the
diffusion-weighted images than on the FLAIR images. In terms of visual
inspection, diffusion-weighted imaging might provide better lesion contrast
than FLAIR imaging for the detection of intraventricular debris and pus (Figs.
2A,
2B,
2C,
2D,
2E,
3A,
3B,
3C,
3D,
3E,
3F, and
3G).

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Fig. 2A 2-month-old boy with acute pyogenic meningitis. T2-weighted
image shows slight dilatation of left occipital horn of lateral ventricle
without findings of intraventricular and periventricular lesion.
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Fig. 2B 2-month-old boy with acute pyogenic meningitis. FLAIR image
shows small area of slight hyperintensity in left occipital horn and slight
hyperintensity along ventricular wall of left occipital horn. Leptomeningeal
hyperintensity is also noted in left frontal region, suggesting
meningitis.
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Fig. 2C 2-month-old boy with acute pyogenic meningitis.
Contrast-enhanced T1-weighted image shows no significant enhancement of
ventricular lining compared with meningeal enhancement in left frontal region,
which is consistent with meningitis.
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Fig. 2D 2-month-old boy with acute pyogenic meningitis.
Diffusion-weighted image reveals areas of intraventricular hyperintensity in
bilateral occipital horn. Right intraventricular lesion is not detected on
other sequence images. Periventricular abnormal signal intensity is
indeterminate.
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Fig. 3A 39-year-old man with AIDS and intracranial tuberculous infection. FLAIR
image shows intraventricular lesions in left occipital horn of lateral
ventricles with areas of hyperintensity along ventricular lining. Alteration
of signal intensity in right occipital horn is minimal. Areas of
hyperintensity suggesting infarction of bilateral basal ganglia and right
frontal region are also seen.
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Fig. 3B 39-year-old man with AIDS and intracranial tuberculous infection.
Contrast-enhanced T1-weighted image shows areas of slight hyperintensity
relative to CSF in bilateral occipital horn. No periventricular enhancement is
seen.
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Fig. 3D 39-year-old man with AIDS and intracranial tuberculous infection. FLAIR
image 10 days after initial study shows newly developed cerebral lesion in
left occipital region adjacent to left occipital horn in which
intraventricular lesions have persisted. Areas of hyperintensity along
ventricular wall are prominent. Dilated lateral ventricles and third ventricle
are also newly seen.
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Fig. 3E 39-year-old man with AIDS and intracranial tuberculous infection.
Contrast-enhanced T1-weighted image 10 days after initial study shows focal
enhancement in left occipital region, suggesting cerebritis. No enhancement of
ventricular wall is noted.
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Fig. 3F 39-year-old man with AIDS and intracranial tuberculous infection.
Diffusion-weighted image 10 days after initial study shows areas of
conspicuous focal hyperintensity in left occipital horn and along ventricular
wall of bilateral occipital horn, which are different from other sequences in
distribution. Hyperintensity in left occipital region suggests newly developed
cerebritis.
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Fig. 3G 39-year-old man with AIDS and intracranial tuberculous infection.
Diffusion-weighted image obtained at pons level 10 days after initial study
shows hyperintensity in dependent portion of dilated fourth ventricle and in
right cerebellopontine cistern, suggesting intraventricular debris and pus and
meningitis, respectively.
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Regarding the diffusion-weighted imaging findings, the lower mean ADC
values of the hyperintense lesions might suggest the presence of material with
restricted water diffusion in the ventricular space, consistent with previous
descriptions of intraventricular debris and pus
[1,
5] (Figs.
1A,
1B,
1C,
1D, and
1E). Intraventricular
hemorrhage should be included in a differential diagnosis of intraventricular
hyperintensity. However, clinical information would probably be helpful for
distinguishing ventriculitis from intraventricular hemorrhage.
FLAIR imaging had the highest detectability rate for periventricular
abnormalities, although this MRI finding is less frequent than
intraventricular debris and pus. When symmetric abnormalities are present, the
possibility of a periventricular inflammatory process should be considered.
Areas of hyperintensity are frequently observed on FLAIR images of the
periventricular white matter, particularly around the anterior and posterior
horns of the ventricles. These areas of hyperintensity are called "caps
and rims" and are considered to suggest age-related chronic ischemic
changes in the white matter that are histologically characterized by myelin
pallor, gliosis, and arteriosclerosis in the caps and subependymal gliosis and
loss of the ependymal lining in the rims
[6].
Furthermore, in the patients with hydrocephalus, the FLAIR images
occasionally showed areas of periventricular hyperintensity in a
circumferential fashion caused by the transependymal migration of CSF
[3]. Interestingly,
contrast-enhanced T1-weighted imaging was less sensitive at detecting
ventricular wall abnormalities compared with the FLAIR and T2-weighted images.
One possible explanation for this discrepancy is that false-positive abnormal
periventricular findings on the FLAIR and T2-weighted images may have been
included among the positive cases or that ventricular wall enhancement arising
from the breakdown of the blood-brain barrier in the ependymal region may
occur during a relatively advanced phase of ventriculitis.
Possible routes through which a pathogen might enter the intraventricular
system include direct implantation secondary to trauma and postsurgical
conditions, such as ventricular catheter placement; contiguous extension, such
as the rupture of a brain abscess and extension into the ventricles; and
hematogenous spread to the subependyma or the choroid plexus
[2,
4,
7]. We postulated that the
backflow of CSF from the extraventricular spaces into the intraventricular
space might be another possible route of infection leading to ventriculitis.
In three MRI studies in three patients, we observed abnormal intensities
located in the fourth ventricle that had signal features identical to those of
the intraventricular debris and pus seen in the lateral ventricles in the
present study (Fig. 3G). We
speculated that the debris and pus may have been conveyed from the lateral
ventricles craniocaudally or from the extraventricular spaces caudocranially
along with the CSF flow. In one of these patients, an additional follow-up MRI
study revealed the development of cerebritis in the posterior lobe adjacent to
the posterior horn of the lateral ventricle, in which the intraventricular
debris and pus had persisted since the time of the initial study (Figs.
3A,
3B,
3C,
3D,
3E,
3F, and
3G). This finding suggests
that the implantation of intraventricular debris and pus in the ventricular
wall might cause ependymitis, leading to cerebritis or the formation of a
brain abscess.
A blood clot in the ventricular system, caused by CSF backflow, is
sometimes observed in cases of subarachnoid hemorrhage. This phenomenon is
thought to arise from the alteration of pulsatile CSF flow dynamics by reduced
compliance of the intracranial subarachnoid spaces as a result of the
hemorrhage [8]. Other
abnormalities of the subarachnoid space, including infection, might also
contribute to changes in CSF flow. This concept might explain the observation
that ventriculitis is often associated with meningitis.
Choroid plexitis is thought to be another MRI finding associated with
ventriculitis. Imaging findings for choroid plexitis have been well described
and include a poorly defined margin of a swollen choroid plexus and contrast
enhancement of the choroid plexus
[9]. We observed choroid
plexitis on five contrast-enhanced T1-weighted scans obtained in four
patients. In each case, the MR images showed asymmetric enlargement of the
choroid plexus. However, abnormal choroid plexus findings could not be
identified with certainty on the diffusion-weighted and FLAIR images, possibly
because the abnormal intensities produced by the intraventricular debris and
pus were too bright, making it difficult to differentiate them from findings
indicating choroid plexitis.
The present study has at least three major limitations. First, the number
of patients was small. However, this small series of patients diagnosed as
having ventriculitis over a 5-year period reflects the rarity of this disease.
Second, the presence of a causative organism in CSF drained directly from the
lateral ventricles was not confirmed, except in three patients who underwent
surgical interventions because of their postsurgical status for other
indications (tumor resection, aneurysm clipping, and existing ventriculostomy
tube for shunt). Although prompt treatment of ventriculitis is critical,
surgical intervention has not been established as a treatment of first choice,
especially for early stage ventriculitis
[10]. We think that the
laboratory findings for CSF obtained from a lumbar puncture, the clinical
follow-up information, and the previously reported MRI features were
sufficient to diagnose ventriculitis in the present study. Third, our study
had a selection bias because cases with false-negative MRI findings were not
included. However, if patients with ventriculitis have negative MRI findings,
it is difficult to diagnose ventriculitis based only on clinical findings. No
false-positive cases occurred in the present study, possibly implying that MRI
contributes significantly to the diagnosis of ventriculitis.
In conclusion, diffusion-weighted and FLAIR imaging may be valuable MRI
sequences for detecting intraventricular debris and pus, suggestive of
ventriculitis. Diffusion-weighted imaging may be particularly useful for
recognizing intraventricular debris and pus because of the conspicuity of the
lesions, drawing attention to the existence of ventriculitis. FLAIR imaging
might be more valuable than contrast-enhanced T1-weighted imaging for
depicting periventricular abnormalities, the second most common MRI feature of
ventriculitis.
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