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1 i 6i
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Demonstration of Reversible Cerebral Lesions Child with Hypertensive Encephalopathy Caused by Wilms’ Tumor
in a
MR
Dean
J. Shanley1
and Cheryl
L. Sisler
We report a case of reversible MR abnormalities involving the occipital lobe cortex and subcortical white matter bilaterally in a patient with severe systemic arterial hypertension associated described
with a Wilms’ tumor. Similar findings have in patients with the preeclampsia-eclampsia
drome and hypertensive encephalopathy [1-5]. hypertension has been attributed to elevated either
due
to tumor
renovascular though
production
insufticiency
arterial
of renin
caused
hypertension
of cerebral
cephalopathy
abnormalities
Wilms-related
renin activity or in response to
mass,
Al-
in as many
as 50%
of
occurs caused
in these patients
been syn-
by the tumor
cases of Wilms’ tumor, to our knowledge tion
by hypertensive
A 5-year-old mass
of vomiting
during
showed
matter of the occipital
was discontinued motensive.
and blood
intermittent
examination pressure
abdominal
of around
i2 x 17 cm mass in the right Wilms’ tumor with associated
kidney,
discomfort
a large right-sided
and
consti-
abdominal a of
was made. Before anti-
hypertensive therapy was started, the patient had several tonic-clonic seizures, which were followed by periods of deep somnolence accompanied by a transient positive Babinski’s sign on the left. No
persistent neurologic examination showed
in cerebral
No pathologic
enhancement
seizures
and the patient have occurred.
MR images of the head showed
complete
has remained
One-month
resolution
nor-
follow-up
of the original
Discussion
160/i 20 mm Hg. CT showed and a presumptive diagnosis
hypertension
resulting
en-
has not been described.
showed
lobes bilaterally.
after surgery,
No further
have been described in patients and hypertensive encephalopathy [1 -5]. Reversible white matter changes are commonly observed in patients with toxemia of pregnancy and hypertensive encephalopathy and have been attributed to transient dysfunction of cerebral autoregulation and alteration of the normal blood-brain barrier [1 2, 5]. The precise cause of A variety
girl had
months
was detected after IV administration of gadopentetate dimeglumine. Before surgical resection of the renal mass, the hypertension was controlled with oral medication. The pathologic diagnosis was Wilms’ tumor, stage II, with a favorable histology. Antihypertensive therapy
with
Physical
the past several
MR images (Figs. 1 B and iC) obtained the next day areas of increased signal in the cortex and subcortical white
shrinkage.
abnormalities.
the MR demonstra-
Case Report pation.
Report
deficits were detected. Postictal funduscopic no evidence of papilledema, and visual fields
of CNS
toxemia
lesions
of pregnancy
,
these
abnormalities
hypoxic
is uncertain.
ischemia,
rhage,
perivascular
rhage,
have been
vasculopathy,
microinfarcts, implicated
Multiple
factors,
perivascular
and intracerebral
on the basis
including
microhemor-
of autopsy
hemorfindings
were normal. CT of the head (Fig. IA) showed areas of decreased
[6].
density in the occipital lobes bilaterally. which was attributed to poor nutritional
Severe hypertensive episodes may cause an exaggerated autoregulatory response by the cerebral vessels resulting in
Received September 16, 1991 accepted ‘Both authors: Department of Radiology, AJR 166:1161-1162,
The brain appeared intake and recurrent
atrophic, episodes
after revision October 21, 1991. Tripler Army Medical Center, Honolulu,
May 1992 0361-803X/92/1585-1
161 © American Roentgen
HI 96859. Ray Society
Address
reprint
requests
to D. J. Shanley.
SHANLEY
Downloaded from www.ajronline.org by 182.72.70.10 on 10/17/15 from IP address 182.72.70.10. Copyright ARRS. For personal use only; all rights reserved
1162
AND
SISLER
AJR:158,
Fig. 1.-5-year-old giri with arterial hypertension associated with Wilms’ tumor. A, Unenhanced CT scan shows decreased attenuation in occipital lobes (arrows) bilaterally. B and C, Proton-density-weighted, 2500/30 (TR/TE) (B), and T2-weighted, 2500/90 (C), MR images show increased
signal (arrows)
May 1992
in both gray and
white matter of occipital lobes. MR images obtained I month later showed complete resolution of original abnormalities.
gray matter. Recent reports [7, 8] describing angiographic findings in patients with eclampsia and reversible cerebral abnormalities on MR provided further evidence in support of
malities in our patient, involving mostly the white matter of the occipital lobes and a lesser degree of cortical involvement, supports the concept of a dual mechanism in the development of increased brain water content; alterations in the bloodbrain barrier contributed to the development of vasogenic edema, and vasoconstriction-induced ischemia resulted in
a vasoconstrictive
cytotoxic
diffuse vasoconstriction [3, 5]. The vasoconstriction cerebral ischemia and cytotoxic edema, manifested
images as areas of increased
cause.
signal involving
Dysfunction
leads to on MR
both white and
of the autoregulatory
edema.
Both patterns
of edema were reversible
mechanism, in part due to the vasoconstriction-induced ischemia and persistent hypertension, leads to an alteration in the blood-brain barrier and extravasation of fluid into the surrounding brain parenchyma. This pattern of vasogenic
our case, similar to previously reported cases of reversible brain lesions in eclampsia and hypertensive encephalopathy.
edema
REFERENCES
is also seen on MR images
as areas
of increased
signal and is classically confined to the white matter. Thus, there is a mechanism for the development of cytotoxic edema (vasoconstriction and ischemia) and vasogenic edema (disruption of the blood-brain barrier) in the setting of severe hypertensive episodes. Separation of these two patterns of edema may not always be possible with MR, and it is likely that both mechanisms are responsible for the signal abnormalities seen in patients with eclampsia and hypertensive
encephalopathy. The striking similarities in the pattern, distribution, and reversibility of MR abnormalities in our case of Wilms-related hypertension and in patients with toxemia of pregnancy sug-
gest a similar CNS response
to severe systemic
The presence
and cytotoxic
patterns
is a common
finding
involving
the
of vasogenic occipital
lobes
hypertension. of edema in patients
eclampsia [1 2, 5]. Preferential involvement of the postenor cerebral circulation is not readily explainable in our case or in the previously reported cases of CNS abnormalities in patients with eclampsia [5]. Localization of the MR abnorwith
,
1 . Schwaighofer ible brain
BW, Hesselink JR. Healy ME. MR demonstration abnormalities in eclampsia. J Comput Assist
in
of reversTomogr
1989;13:310-312 2. Raroque HG, Orrison WW, Rosenberg GA. Neurologic involvement in toxemia of pregnancy: reversible MRI lesions. Neurology 1990;40: 167-1 69 3. Hauser RA, Lacey DM, Knight MR. Hypertensive encephalopathy: magnetic resonance imaging demonstration of reversible cortical and white matter lesions. Arch Neurol 1988;45 :1078-1083 4. Gibby WA, Stecker MM, Goldberg HI, et al. Reversal of white mailer edema in hypertensive encephalopathy. AJNR 1989;10:S78 5. Saunders TG, Clayman DA, Sanchez-Ramos L, Vines FS, Russo L. Brain in eclampsia: MR imaging with clinical correlation. Radiology 1991;180:475-478 6. Richards A, Graham D, Bullock A. Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy. J Neurol Neurosurg Psychiatry 1988;51 :416-421 7. Will AD, Lewis KL, Hinshaw DB, et al. Cerebral vasoconstriction in toxemia. Neurology 1987;37: 1555-1 557 8. Lewis LK, Hinshaw DB, Will AD, Hasso AN, Thompson JR. CT and angiographic correlation of severe neurological disease in toxemia of pregnancy. Neuroradiology 1988;30:59-64
1 i 6i
Case .-
(u
,
c
#{149}
7
.4
1
,
.
:
%I
.:
Demonstration of Reversible Cerebral Lesions Child with Hypertensive Encephalopathy Caused by Wilms’ Tumor
in a
MR
Dean
J. Shanley1
and Cheryl
L. Sisler
We report a case of reversible MR abnormalities involving the occipital lobe cortex and subcortical white matter bilaterally in a patient with severe systemic arterial hypertension associated described
with a Wilms’ tumor. Similar findings have in patients with the preeclampsia-eclampsia
drome and hypertensive encephalopathy [1-5]. hypertension has been attributed to elevated either
due
to tumor
renovascular though
production
insufticiency
arterial
of renin
caused
hypertension
of cerebral
cephalopathy
abnormalities
Wilms-related
renin activity or in response to
mass,
Al-
in as many
as 50%
of
occurs caused
in these patients
been syn-
by the tumor
cases of Wilms’ tumor, to our knowledge tion
by hypertensive
A 5-year-old mass
of vomiting
during
showed
matter of the occipital
was discontinued motensive.
and blood
intermittent
examination pressure
abdominal
of around
i2 x 17 cm mass in the right Wilms’ tumor with associated
kidney,
discomfort
a large right-sided
and
consti-
abdominal a of
was made. Before anti-
hypertensive therapy was started, the patient had several tonic-clonic seizures, which were followed by periods of deep somnolence accompanied by a transient positive Babinski’s sign on the left. No
persistent neurologic examination showed
in cerebral
No pathologic
enhancement
seizures
and the patient have occurred.
MR images of the head showed
complete
has remained
One-month
resolution
nor-
follow-up
of the original
Discussion
160/i 20 mm Hg. CT showed and a presumptive diagnosis
hypertension
resulting
en-
has not been described.
showed
lobes bilaterally.
after surgery,
No further
have been described in patients and hypertensive encephalopathy [1 -5]. Reversible white matter changes are commonly observed in patients with toxemia of pregnancy and hypertensive encephalopathy and have been attributed to transient dysfunction of cerebral autoregulation and alteration of the normal blood-brain barrier [1 2, 5]. The precise cause of A variety
girl had
months
was detected after IV administration of gadopentetate dimeglumine. Before surgical resection of the renal mass, the hypertension was controlled with oral medication. The pathologic diagnosis was Wilms’ tumor, stage II, with a favorable histology. Antihypertensive therapy
with
Physical
the past several
MR images (Figs. 1 B and iC) obtained the next day areas of increased signal in the cortex and subcortical white
shrinkage.
abnormalities.
the MR demonstra-
Case Report pation.
Report
deficits were detected. Postictal funduscopic no evidence of papilledema, and visual fields
of CNS
toxemia
lesions
of pregnancy
,
these
abnormalities
hypoxic
is uncertain.
ischemia,
rhage,
perivascular
rhage,
have been
vasculopathy,
microinfarcts, implicated
Multiple
factors,
perivascular
and intracerebral
on the basis
including
microhemor-
of autopsy
hemorfindings
were normal. CT of the head (Fig. IA) showed areas of decreased
[6].
density in the occipital lobes bilaterally. which was attributed to poor nutritional
Severe hypertensive episodes may cause an exaggerated autoregulatory response by the cerebral vessels resulting in
Received September 16, 1991 accepted ‘Both authors: Department of Radiology, AJR 166:1161-1162,
The brain appeared intake and recurrent
atrophic, episodes
after revision October 21, 1991. Tripler Army Medical Center, Honolulu,
May 1992 0361-803X/92/1585-1
161 © American Roentgen
HI 96859. Ray Society
Address
reprint
requests
to D. J. Shanley.
SHANLEY
Downloaded from www.ajronline.org by 182.72.70.10 on 10/17/15 from IP address 182.72.70.10. Copyright ARRS. For personal use only; all rights reserved
1162
AND
SISLER
AJR:158,
Fig. 1.-5-year-old giri with arterial hypertension associated with Wilms’ tumor. A, Unenhanced CT scan shows decreased attenuation in occipital lobes (arrows) bilaterally. B and C, Proton-density-weighted, 2500/30 (TR/TE) (B), and T2-weighted, 2500/90 (C), MR images show increased
signal (arrows)
May 1992
in both gray and
white matter of occipital lobes. MR images obtained I month later showed complete resolution of original abnormalities.
gray matter. Recent reports [7, 8] describing angiographic findings in patients with eclampsia and reversible cerebral abnormalities on MR provided further evidence in support of
malities in our patient, involving mostly the white matter of the occipital lobes and a lesser degree of cortical involvement, supports the concept of a dual mechanism in the development of increased brain water content; alterations in the bloodbrain barrier contributed to the development of vasogenic edema, and vasoconstriction-induced ischemia resulted in
a vasoconstrictive
cytotoxic
diffuse vasoconstriction [3, 5]. The vasoconstriction cerebral ischemia and cytotoxic edema, manifested
images as areas of increased
cause.
signal involving
Dysfunction
leads to on MR
both white and
of the autoregulatory
edema.
Both patterns
of edema were reversible
mechanism, in part due to the vasoconstriction-induced ischemia and persistent hypertension, leads to an alteration in the blood-brain barrier and extravasation of fluid into the surrounding brain parenchyma. This pattern of vasogenic
our case, similar to previously reported cases of reversible brain lesions in eclampsia and hypertensive encephalopathy.
edema
REFERENCES
is also seen on MR images
as areas
of increased
signal and is classically confined to the white matter. Thus, there is a mechanism for the development of cytotoxic edema (vasoconstriction and ischemia) and vasogenic edema (disruption of the blood-brain barrier) in the setting of severe hypertensive episodes. Separation of these two patterns of edema may not always be possible with MR, and it is likely that both mechanisms are responsible for the signal abnormalities seen in patients with eclampsia and hypertensive
encephalopathy. The striking similarities in the pattern, distribution, and reversibility of MR abnormalities in our case of Wilms-related hypertension and in patients with toxemia of pregnancy sug-
gest a similar CNS response
to severe systemic
The presence
and cytotoxic
patterns
is a common
finding
involving
the
of vasogenic occipital
lobes
hypertension. of edema in patients
eclampsia [1 2, 5]. Preferential involvement of the postenor cerebral circulation is not readily explainable in our case or in the previously reported cases of CNS abnormalities in patients with eclampsia [5]. Localization of the MR abnorwith
,
1 . Schwaighofer ible brain
BW, Hesselink JR. Healy ME. MR demonstration abnormalities in eclampsia. J Comput Assist
in
of reversTomogr
1989;13:310-312 2. Raroque HG, Orrison WW, Rosenberg GA. Neurologic involvement in toxemia of pregnancy: reversible MRI lesions. Neurology 1990;40: 167-1 69 3. Hauser RA, Lacey DM, Knight MR. Hypertensive encephalopathy: magnetic resonance imaging demonstration of reversible cortical and white matter lesions. Arch Neurol 1988;45 :1078-1083 4. Gibby WA, Stecker MM, Goldberg HI, et al. Reversal of white mailer edema in hypertensive encephalopathy. AJNR 1989;10:S78 5. Saunders TG, Clayman DA, Sanchez-Ramos L, Vines FS, Russo L. Brain in eclampsia: MR imaging with clinical correlation. Radiology 1991;180:475-478 6. Richards A, Graham D, Bullock A. Clinicopathological study of neurological complications due to hypertensive disorders of pregnancy. J Neurol Neurosurg Psychiatry 1988;51 :416-421 7. Will AD, Lewis KL, Hinshaw DB, et al. Cerebral vasoconstriction in toxemia. Neurology 1987;37: 1555-1 557 8. Lewis LK, Hinshaw DB, Will AD, Hasso AN, Thompson JR. CT and angiographic correlation of severe neurological disease in toxemia of pregnancy. Neuroradiology 1988;30:59-64
