NEUROIMAGING ON DELAYED POSTANOXICENCEPHALOPATHY WITH LESIONS LOCALIZED INBASAL 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- tremities, hyperreflexia, and positive pathologicaltension with myocardial infarction. Sixteen days after reflexes several days or weeks after the anoxic epi-the episode, she showed bradykinesia, gait distur- sode (1–4). Delayed postanoxic encephalopathy hasbance, and postural tremor. MRI revealed low signa been reported in patients with carbon monoxide in-intensities in the bilateral caudate nuclei and puta- toxication (4, 5), cardiac arrest, strangling (1, 3), an-men on the T1-weighted image and high signal inten- esthetic accident (4), and so on (2, 4). Most previoussities on the T2-weighted image. PET with 18F-FDG reports on delayed anoxic changes have describedrevealed a severe decrease in glucose metabolism in cerebral white matter or laminar cortical lesions (2,bilateral basal ganglia. It is concluded that prolonged 4, 6, 7). Three reports, however, described lesions lo-hypotension may induce localized delayed anoxic le- calized in basal ganglia, confirmed by pathologicalsions in basal ganglia. Elsevier Science Inc., 1998 examination (1), computed tomography (CT), or

magnetic resonance imaging (MRI) (3, 8), but posi-KEY WORDS: tron emission tomography (PET) was not performed.

We report here a patient with delayed postanoxic en-Delayed anoxic encephalopathy; Magnetic resonanceimaging; Positron emission tomography; Basal ganglia cephalopathy following myocardial infarction who

developed bilateral lesions in basal ganglia alone,not in white matter or cortex on CT and MRI, with

INTRODUCTION glucose hypometabolism in the lesions on PET.

In delayed postanoxic encephalopathy, patients suf-fer from transient unconsciousness during an anoxic

CASE REPORTepisode, followed by a period with no neurologicalabnormalities, and then develop disorientation, am- A 59-year-old woman suddenly suffered from nauseanesia, depression, confusion, akinetic mutism, uri- and chest oppression. She gradually lost conscious-nary incontinence, Parkinsonism, ataxia of the ex- 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 30From the Department of Neurology (W.T., Y.O., Shu.T., F.Y.,minutes. After resuscitation, her systolic blood pres-Shi.T., Y.S.), Tokai University School of Medicine, Isehara, Kana-

gawa, Japan, HIMEDIC Imaging Center at Lake Yamanakako sure gradually returned to approximately 60 mm Hg,(Shi.T.), Yamanakako, Yamanashi, Japan, and the Department of her consciousness level gradually improved, and sheNeurology (T.K.), Chigasaki Tokusyukai Hospital, Chigasaki, Ka-

could speak within 1 hour. Three hours later, shenagawa, Japan.Address correspondence and reprint requests to: Yukito Shi- was completely alert. She was diagnosed as having

nohara, M.D., Department of Neurology, Tokai University Schoolsubendomyocardial infarction, based on an ST-T de-of Medicine, Isehara, Kanagawa 259-11, Japan.

Received March 10, 1997; accepted May 2, 1997. pression and inverted T wave on electrocardiogram

CLINICAL IMAGING 1998;22:188–191 Elsevier Science Inc., 1998. All rights reserved. 0899-7071/98/$19.00655 Avenue of the Americas, New York, NY 10010 PII S0899-7071(97)00120-4

189MAY/JUNE 1998 NEUROIMAGING ON DELAYED ANOXIC ENCEPHALOPATHY

FIGURE 1. (A) CT findings 2 hours after the anoxic episode. No abnormality is apparent in basal ganglia. (B) CT findingson day 28 after the anoxic episode. Low density areas are apparent in bilateral basal ganglia. (C) MRI findings on day 52after the anoxic episode. T1-weighted image shows low signal intensities in the putamen bilaterally. (D) T2-weighted imageshows high signal intensities in the caudate nuclei and putamen bilaterally. There are no obvious cortical and white matterlesions.

190 TAKAHASHI ET AL. CLINICAL IMAGING VOL. 22, NO. 3

TABLE 1. Regional CMRglc (mg/100g/min) in OurPatient and Normal Subjects

Our patientNormal subjects

(n 5 34)

Region Left Right Left Right

Frontal cortex 9.0 8.8 9.7 6 1.4 9.8 6 1.6Parietal cortex 8.5 9.7 9.0 6 1.6 8.7 6 1.6Temporal cortex 11.6 9.7 9.3 6 1.1 9.6 6 1.2Occipital cortex 11.8 11.1 10.5 6 1.9 10.5 6 1.5Cerebral white matter 1.7 1.9 2.4 6 0.5 2.4 6 0.5Caudate nucleus 6.4 5.0 10.3 6 1.7 10.1 6 1.6Putamen 6.6 3.6 10.9 6 1.4 10.5 6 1.5Thalamus 9.6 9.7 10.3 6 1.5 10.2 6 1.5Cerebellum 7.6 7.4 6.9 6 1.1 6.8 6 1.1

Abbreviation: CMRglc 5 cerebral metabolic rate of glucose.

55 6 5 years (Figure 2; Table 1). However, CMRglc val-FIGURE 2. PET with 18F-FDG on day 63 after the anoxicues in cerebral cortex, thalamus, or cerebellum wereepisode. CMRglc is severely decreased in bilateral basal

ganglia. within normal ranges. With administration of 150 mgper day of amantadine hydrochloride and physicaltherapy, the patient’s tremor, bradykinesia, and gait

(ECG). She revealed no abnormality on CT scan per- disturbance were gradually ameliorated, and she couldformed 2 hours after the anoxic episode (Figure 1A) walk smoothly within 4 months after the anoxic epi-and showed no neurological deficit on the second sode. MRI on day 115 showed decreased signal ab-day of admission. On day 16 after the episode, she normalities in bilateral caudate nuclei and putamen.developed postural tremor of her left hand and gaitdisturbance. Since these neurological manifestations

DISCUSSIONgradually worsened, she visited our hospital on day48 after the episode. She was alert and well-oriented. In our patient, neurological symptoms appeared onMini-mental examination showed full points. Cra- day 16 after the anoxic episode, and the first CT scannial nerves, including eye movements, were not dis- showed no low-density region in basal ganglia. MRIturbed. She showed postural and kinetic tremor of on day 52 revealed low signal intensities in the cau-her left hand, dysarthria, bradykinesia, and small- date nuclei and putamen bilaterally on the T1-stepped gait. Deep tendon reflexes were present. weighted image and high signal intensities in theThere was no weakness or sensory deficit to touch, same regions on the T2-weighted image, without ab-pain, temperature, or vibration. normal signals in the cerebral cortex, the hippocam-

CT scan performed at the nearby hospital on day pus, or the cerebral white matter. Most previous re-28 after the anoxic episode showed low-density ar- ports on delayed postanoxic encephalopathy (2, 4, 6,eas in bilateral basal ganglia (Figure 1B). MRI with a 7) have described cerebral white matter or laminar1.0-T superconducting magnet on day 52 after the cortical lesions, though there are three reports (1, 3,anoxic episode revealed low and high signal intensit- 8) of lesions localized in basal ganglia, as in our case.ies on T1 (TR, 500 msec; TE, 20 msec)– and T2 (TR, Interestingly, the lesions visualized by MRI in acute3000 msec; TE, 90 msec)–weighted images, respec- postanoxic encephalopathy are distributed in thetively, in bilateral caudate nuclei and putamen. Cor- caudate nucleus, putamen, or globus pallidus (6, 7),tical, hippocampal, and white matter lesions were in accordance with our findings. However, those re-not apparent (Figures 1C and 1D). PET (ECAT EX- ports described high signal intensities on both T1-ACT, Siemens CTI) was performed after intravenous and T2-weighted images (6, 7), which is differentinjection of 7 mCi of 18F-2-fluoro-2-deoxy-D-glucose from our result. The lesions in basal ganglia in acute(FDG) on day 63 after the anoxic episode. Regional postanoxic encephalopathy have been reported to re-cerebral metabolic rate of glucose (CMRglc) was re- flect petechial hemorrhage (7) or deposition of fat-duced in bilateral caudate nuclei and putamen with laden macrophages (6, 7), but those in our patientgreater reduction on the right side and in cerebral seem to represent mainly necrotic changes based onwhite matter when compared with the CMRglc val- the intensities in the T1- and T2-weighted images.

We speculate that both acute and delayed postanoxicues obtained from 34 healthy volunteers with ages of

191MAY/JUNE 1998 NEUROIMAGING ON DELAYED ANOXIC ENCEPHALOPATHY

2. Ginsberg MD, Hedley-Whyte TE, Richardson EP Jr. Hypoxic-encephalopathies may result in a variety of lesions,ischemic leukoencephalopathy in man. Arch Neurol 1976;

depending on the causal anoxic condition and its se- 33:5–14.verity. Auer and Siesjo (9) reported that the severity

3. Hori A, Hirose G, Kataoka S, Tsukada K, Furui K, Tanami H.and distribution of neuronal necrosis are different in Delayed postanoxic encephalopathy after strangulation: serial

neuroradiological and neurochemical studies. Arch Neurolischemia, hypoglycemia, and epilepsy, supporting1991;48:871–874.the idea that lesions may be variable depending on

4. Plum F, Posner JB, Hain RF. Delayed neurological deteriora-the underlying anoxic condition, such as cardiac ar-tion after anoxia. Arch Intern Med 1962;110:56–63.rest, prolonged hypotension, or hypoxemia. In our

5. Brucher JM. Neuropathological problems posed by carbonpatient, prolonged hypotension appeared to havemonoxide poisoning and anoxia. Prog Brain Res 1967;24:75–produced delayed lesions in basal ganglia. 100.

Regional cerebral blood flow (rCBF), regional glu-6. Sawada H, Udaka F, Seriu N, Shindou K, Kameyama M, Tsuji-

cose metabolic rate (CMRglc), or oxygen metabolism mura M. MRI demonstration of cortical laminar necrosis andhave been measured by PET in patients with acute delayed white matter injury in anoxic encephalopathy. Neur-

oradiology 1990;32:319–321.postanoxic encephalopathy (10–12), but there has7. Takahashi S, Higano S, Ishii K, Matsumoto K, Sakamoto K,been no PET study on delayed postanoxic encepha-

Iwasaki Y, Suzuki M. Hypoxic brain damage: cortical laminarlopathy. In acute postanoxic encephalopathy, CMRglcnecrosis and delayed changes in white matter at sequential

was reduced in cortex (10, 11) or in striatum, thala- MR imaging. Radiology 1993;189:449–456.mus, white matter, and cerebellumin addition to the

8. Yoshida T. A case of delayed postanoxic encephalopathycortex (12). In our patient, however, CMRglc in the with bilateral striatal lesions. Neurol Psychiat Brain Res

1993;1:143–144.caudate nucleus and the putamen was severely re-duced without change in the cerebral cortex, thala- 9. Auer RN, Siesjo BK. Biological differences between ischemia,

hypoglycemia, and epilepsy. Ann Neurol 1988;24:699–707.mus, or cerebellum. These findings may suggest thatcortex does not show subclinical hypometabolic 10. DeVolder AG, Goffinet AM, Bol A, Michel C, Barsy TD, Lat-

erre C. Brain glucose metabolism in postanoxic syndrome:changes after prolonged hypotension and that thepositron emission tomographic study. Arch Neurol 1990;distribution of the hypometabolic changes is not 47:197–204.

well explained by so-called ischemic vulnerability11. Rudolf J, Beil C, Heiss W-D. Regional cerebral glucose metabo-(13). The mechanism of the specific vulnerability of lism in postanoxic syndrome: evidence for prognostic sensi-

the basal ganglia in our patient is unclear. Further tivity? J Cereb Blood Flow Metab 1993;13(Suppl 1):S391.studies, such as a receptor binding study, might be 12. DeReuck J, Decoo D, Vienne J, Strijckmans K, Lemahieu I. Sig-

nificance of white matter lucencies in posthypoxic-ischemicinformative.encephalopathy: comparison of clinical status and of com-puted and positron emission tomographic findings. Eur Neu-rol 1992;32:334–339.REFERENCES

13. Pulsinelli WA. Selective neuronal vulnerability: morphologi-cal and molecular characteristics. Prog Brain Res 1985;1. Dooling EC, Richardson EP Jr. Delayed encephalopathy after63:29–37.strangling. Arch Neurol 1976;33:196–199.