NEUROIMAGING ON DELAYED POSTANOXIC
ENCEPHALOPATHY WITH LESIONS LOCALIZED IN
BASAL GANGLIA
WAKOH TAKAHASHI, MD, YOUICHI OHNUKI, MD,
SHUNYA TAKIZAWA, MD, FUMIHITO YOSHII, MD,
SHIGEHARU TAKAGI, MD, TETSUMASA KAMEI, MD,
AND YUKITO SHINOHARA, MD
A 59-year-old woman suffered from prolonged hypo-
tension with myocardial infarction. Sixteen days after
the episode, she showed bradykinesia, gait distur-
bance, and postural tremor. MRI revealed low signa
intensities in the bilateral caudate nuclei and puta-
men on the T1-weighted image and high signal inten-
sities on the T2-weighted image. PET with 18F-FDG
revealed a severe decrease in glucose metabolism in
bilateral basal ganglia. It is concluded that prolonged
hypotension may induce localized delayed anoxic le-
sions in basal ganglia.  Elsevier Science Inc., 1998
KEY WORDS:
Delayed anoxic encephalopathy; Magnetic resonance
imaging; Positron emission tomography; Basal ganglia
INTRODUCTION
In delayed postanoxic encephalopathy, patients suf-
fer from transient unconsciousness during an anoxic
episode, followed by a period with no neurological
abnormalities, and then develop disorientation, am-
nesia, depression, confusion, akinetic mutism, uri-
nary incontinence, Parkinsonism, ataxia of the ex-
From the Department of Neurology (W.T., Y.O., Shu.T., F.Y.,
Shi.T., Y.S.), Tokai University School of Medicine, Isehara, Kana-
gawa, Japan, HIMEDIC Imaging Center at Lake Yamanakako
(Shi.T.), Yamanakako, Yamanashi, Japan, and the Department of
Neurology (T.K.), Chigasaki Tokusyukai Hospital, Chigasaki, Ka-
nagawa, Japan.
Address correspondence and reprint requests to: Yukito Shi-
nohara, M.D., Department of Neurology, Tokai University School
of Medicine, Isehara, Kanagawa 259-11, Japan.
Received March 10, 1997; accepted May 2, 1997.
CLINICAL IMAGING 1998;22:188–191
 Elsevier Science Inc., 1998. All rights reserved.
655 Avenue of the Americas, New York, NY 10010
tremities, hyperreflexia, and positive pathological
reflexes several days or weeks after the anoxic epi-
sode (1–4). Delayed postanoxic encephalopathy has
been reported in patients with carbon monoxide in-
toxication (4, 5), cardiac arrest, strangling (1, 3), an-
esthetic accident (4), and so on (2, 4). Most previous
reports on delayed anoxic changes have described
cerebral white matter or laminar cortical lesions (2,
4, 6, 7). Three reports, however, described lesions lo-
calized in basal ganglia, confirmed by pathological
examination (1), computed tomography (CT), or
magnetic resonance imaging (MRI) (3, 8), but posi-
tron emission tomography (PET) was not performed.
We report here a patient with delayed postanoxic en-
cephalopathy following myocardial infarction who
developed bilateral lesions in basal ganglia alone,
not in white matter or cortex on CT and MRI, with
glucose hypometabolism in the lesions on PET.
CASE REPORT
A 59-year-old woman suddenly suffered from nausea
and chest oppression. She gradually lost conscious-
ness and was taken to a nearby hospital. On admis-
sion, she was in a coma, her radial pulse was not pal-
pable, and her respiration was very shallow for 30
minutes. After resuscitation, her systolic blood pres-
sure gradually returned to approximately 60 mm Hg,
her consciousness level gradually improved, and she
could speak within 1 hour. Three hours later, she
was completely alert. She was diagnosed as having
subendomyocardial infarction, based on an ST-T de-
pression and inverted T wave on electrocardiogram
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MAY/JUNE 1998 NEUROIMAGING ON DELAYED ANOXIC ENCEPHALOPATHY 189

FIGURE 1. (A) CT findings 2 hours after the anoxic episode. No abnormality is apparent in basal ganglia. (B) CT findings
on day 28 after the anoxic episode. Low density areas are apparent in bilateral basal ganglia. (C) MRI findings on day 52
after the anoxic episode. T1-weighted image shows low signal intensities in the putamen bilaterally. (D) T2-weighted image
shows high signal intensities in the caudate nuclei and putamen bilaterally. There are no obvious cortical and white matter
lesions.
190 TAKAHASHI ET AL. CLINICAL IMAGING VOL. 22, NO. 3

TABLE 1. Regional CMRglc (mg/100g/min) in Our

Patient and Normal Subjects
Normal subjects
Our patient (n 5 34)
Region Left Right Left Right

Frontal cortex 9.0 8.8 9.7 6 1.4 9.8 6 1.6

Parietal cortex 8.5 9.7 9.0 6 1.6 8.7 6 1.6
Temporal cortex 11.6 9.7 9.3 6 1.1 9.6 6 1.2
Occipital cortex 11.8 11.1 10.5 6 1.9 10.5 6 1.5
Cerebral white matter 1.7 1.9 2.4 6 0.5 2.4 6 0.5
Caudate nucleus 6.4 5.0 10.3 6 1.7 10.1 6 1.6
Putamen 6.6 3.6 10.9 6 1.4 10.5 6 1.5
Thalamus 9.6 9.7 10.3 6 1.5 10.2 6 1.5
Cerebellum 7.6 7.4 6.9 6 1.1 6.8 6 1.1
Abbreviation: CMRglc 5 cerebral metabolic rate of glucose.

FIGURE 2. PET with 18F-FDG on day 63 after the anoxic
episode. CMRglc is severely decreased in bilateral basal
ganglia.
(ECG). She revealed no abnormality on CT scan per-
formed 2 hours after the anoxic episode (Figure 1A)
and showed no neurological deficit on the second
day of admission. On day 16 after the episode, she
developed postural tremor of her left hand and gait
disturbance. Since these neurological manifestations
gradually worsened, she visited our hospital on day
48 after the episode. She was alert and well-oriented.
Mini-mental examination showed full points. Cra-
nial nerves, including eye movements, were not dis-
turbed. She showed postural and kinetic tremor of
her left hand, dysarthria, bradykinesia, and small-
stepped gait. Deep tendon reflexes were present.
There was no weakness or sensory deficit to touch,
pain, temperature, or vibration.
CT scan performed at the nearby hospital on day
28 after the anoxic episode showed low-density ar-
eas in bilateral basal ganglia (Figure 1B). MRI with a
1.0-T superconducting magnet on day 52 after the
anoxic episode revealed low and high signal intensit-
ies on T1 (TR, 500 msec; TE, 20 msec)– and T2 (TR,
3000 msec; TE, 90 msec)–weighted images, respec-
tively, in bilateral caudate nuclei and putamen. Cor-
tical, hippocampal, and white matter lesions were
not apparent (Figures 1C and 1D). PET (ECAT EX-
ACT, Siemens CTI) was performed after intravenous
injection of 7 mCi of 18F-2-fluoro-2-deoxy-D-glucose
(FDG) on day 63 after the anoxic episode. Regional
cerebral metabolic rate of glucose (CMRglc) was re-
duced in bilateral caudate nuclei and putamen with
greater reduction on the right side and in cerebral
white matter when compared with the CMRglc val-
ues obtained from 34 healthy volunteers with ages of
55 6 5 years (Figure 2; Table 1). However, CMRglc val-
ues in cerebral cortex, thalamus, or cerebellum were
within normal ranges. With administration of 150 mg
per day of amantadine hydrochloride and physical
therapy, the patient’s tremor, bradykinesia, and gait
disturbance were gradually ameliorated, and she could
walk smoothly within 4 months after the anoxic epi-
sode. MRI on day 115 showed decreased signal ab-
normalities in bilateral caudate nuclei and putamen.
DISCUSSION
In our patient, neurological symptoms appeared on
day 16 after the anoxic episode, and the first CT scan
showed no low-density region in basal ganglia. MRI
on day 52 revealed low signal intensities in the cau-
date nuclei and putamen bilaterally on the T1-
weighted image and high signal intensities in the
same regions on the T2-weighted image, without ab-
normal signals in the cerebral cortex, the hippocam-
pus, or the cerebral white matter. Most previous re-
ports on delayed postanoxic encephalopathy (2, 4, 6,
7) have described cerebral white matter or laminar
cortical lesions, though there are three reports (1, 3,
8) of lesions localized in basal ganglia, as in our case.
Interestingly, the lesions visualized by MRI in acute
postanoxic encephalopathy are distributed in the
caudate nucleus, putamen, or globus pallidus (6, 7),
in accordance with our findings. However, those re-
ports described high signal intensities on both T1-
and T2-weighted images (6, 7), which is different
from our result. The lesions in basal ganglia in acute
postanoxic encephalopathy have been reported to re-
flect petechial hemorrhage (7) or deposition of fat-
laden macrophages (6, 7), but those in our patient
seem to represent mainly necrotic changes based on
the intensities in the T1- and T2-weighted images.
We speculate that both acute and delayed postanoxic
MAY/JUNE 1998
encephalopathies may result in a variety of lesions,
depending on the causal anoxic condition and its se-
verity. Auer and Siesjö (9) reported that the severity
and distribution of neuronal necrosis are different in
ischemia, hypoglycemia, and epilepsy, supporting
the idea that lesions may be variable depending on
the underlying anoxic condition, such as cardiac ar-
rest, prolonged hypotension, or hypoxemia. In our
patient, prolonged hypotension appeared to have
produced delayed lesions in basal ganglia.
Regional cerebral blood flow (rCBF), regional glu-
cose metabolic rate (CMRglc), or oxygen metabolism
have been measured by PET in patients with acute
postanoxic encephalopathy (10–12), but there has
been no PET study on delayed postanoxic encepha-
lopathy. In acute postanoxic encephalopathy, CMRglc
was reduced in cortex (10, 11) or in striatum, thala-
mus, white matter, and cerebellumin addition to the
cortex (12). In our patient, however, CMRglc in the
caudate nucleus and the putamen was severely re-
duced without change in the cerebral cortex, thala-
mus, or cerebellum. These findings may suggest that
cortex does not show subclinical hypometabolic
changes after prolonged hypotension and that the
distribution of the hypometabolic changes is not
well explained by so-called ischemic vulnerability
(13). The mechanism of the specific vulnerability of
the basal ganglia in our patient is unclear. Further
studies, such as a receptor binding study, might be
informative.
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