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key words: cerebral infarcts, computed tomography, lentiform nucleus, insular ribbon, middle cerebral artery
SUMMARY
The aim of our study is to determine how early and reliably ischemic brain infarcts can be detected on CT scan-
ning. We report two cases of an early CT finding of acute ischemic infarcts where CT examination was obtained
within the first 3 hours of onset of neurological symptoms. CT examination showed blurred outlines and
decreased attenuation of the left lentiform nucleus, loss of the white-gray matter interface in the left insular cor-
tex and left cortical global hypoattenuation with obliteration of left cortical sulci in one patient. In second
patient CT showed the following: hyperdense left middle cerebral artery, loss of clear margins of left lentiform
nucleus, subtle focal cortical hypodensity in the left fronto-parietal area with signs of mass effect in the form of
ventricular compression.
CT is still the first choice in the deferential diagnosis of acute stroke. Although older literature positions have
suggested that CT was negative during the first 48 hours, modern CT technology can demonstrate positive find-
ings even in the first 3 hours of onset. This is important in patients with acute stroke, as thrombolytic therapy
when elected, has to be given within the first 36 hours after onset of symptoms.
To determine how early and reliably ischemic brain infarcts can be detected on CT scanning, we report two
cases of an early CT finding of acute ischemic infarcts where CT examination was obtained within the first 3
hours of onset of neurological symptoms.
Received: 2000.03.08 Correspondence address: Mohamed Abdalla MD, Department of Neuroradiology, Institute of Psychiatry and Neurology,
Accepted: 2000.08.20 Al. Sobieskiego 1/9, 02-957 Warsaw, Poland
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Diagnostics and Medical Technology
attenuation of the left lentiform nucleus, loss of the cells. This shift of water into intracellular compart-
gray-white matter interface in the left insular cortex ment results in cytotoxic edema [6]. This early
(loss of insular ribbon) and left cortical global edema is responsible for early CT findings in acute
hypoattenuation with obliteration of left cortical ischemic infarction.
sulci.
On the other hand, a relatively more tolerant
Case 2 endothelial cells do not manifest histopathological
changes until 4 to 12 hours after ischemic insult.
A 48-year-old man with history of hypertension These cells are responsible for the tight cell junc-
and diabetes noticed sudden weakness in the right tions that make up the blood-brain barrier. With
side of his body. Admitted to neurology clinic, an the break down of that barrier, vasogenic edema
urgent CT was performed within 6 hours. develops where water and protein flood from
intracellular compartments into the extracellular
CT showed the following: space. The x-ray attenuation seen with CT scan-
ning is directly proportional to tissue water con-
hyperdense left middle cerebral artery HDMCA, tent. Any increase in tissue water content results in
loss of clear margins of left lentiform nucleus, decrease in x-ray attenuation. A number of CT
subtle focal cortical hypodensity in the left fron- findings have been identified, which generally
to-parietal area with signs of mass effect in the involve loss of appreciation of the attenuation dif-
form of ventricular compression. ference between gray matter and white matter.
CT is routinely used in diagnosis and evaluation of Obscured boundaries of the lentiform nucleus
the extent of acute cerebral infarct. A few years (pallidum, putamen) which is predominantly gray
ago, the role of CT in the setting of hyperacute matter and the surrounding white matter tracks
stroke was only to exclude other similar conditions from the internal and external capsules. It is
mimicking acute ischemic stroke (subarachnoid or more obvious in the putamen, therefore the lat-
intracerebral hemorrhage, tumor, etc.). eral margin of the internal capsule is the first to
be blurred. This sign was first described by
Now the role of CT is changing from peripheral to Tomura et al. in 1988 [1] as slight hypoattenua-
more central one. It is the most widely available tion recognized as early as 1 hour after the onset
tool in determining which patients are eligible for of symptoms, the deep MCA territory seems
specific anti-stroke treatment. Although older litera- extremely sensitive because the lenticulostriate
ture suggested that CT was negative during the first arteries supply end zone territories and account
48 hours, more recent studies have demonstrated for this sign.
positive findings even in the first 3 hours of onset.
Any understanding of imaging changes in diagnostic Loss of clear margin between the insular cortex
methods after the ischemic insult requires a famil- (gray matter) and external and extreme capsule
iarity with pathophysiological changes that ensue (white matter) loss of insular ribbon, anatomi-
after interruption of blood supply. cally, insular ribbon refers to the claustrum,
extreme capsule and insular cortex. This sign,
Normal cerebral blood flow remains within the however, is a frequent early sign of ischemia
range of 5055 ml/100 g of brain tissues/minute. If requiring high CT resolution because of the prox-
cerebral blood flow decreases to 15 ml/100 g/min, imity and delicate arrangement of those struc-
a loss of electrical activity occurs within seconds tures. It was first described by Truwit et al. in
[4,5]. Within one hour there is a depletion of cellu- 1990. The blood supply to the insular ribbon is
lar energy (ATP) with shift to anaerobic glycolysis. mainly provided by claustral arteries arising from
Therefore, ion pumps within the cell membrane the M2 segment of the MCA.
are unable to continue their function. As the ATP
level drops and membrane potential falls, there is Focal cortical hypoattenuation. Due to focal cor-
an influx of sodium and potassium into the cells. tical edema lead to loss of normal attenuation
Water follows this ionic influx, in addition tissue between cortical gray and white matter, with
acidosis resulting from anaerobic metabolism fur- compression of CSF spaces leading to relative
ther accelerates osmotic water diffusion into the obliteration of cortical sulci. Hemispheric sulcal
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Abdalla M et al Hyperacute infarction: early CT findings
Figure 1. a) CT scan done 3 hours after the onset of neurological symptoms shows blurred lateral margin on the left internal capsule with obliteration
of the left lateral sulcus. b) Indistinct demarcation between white and gray matter of the left cerebral cortex with effacement of cortical sulci
in the fronto-temporal area. c) Control CT after 5 days after the onset of symptoms shows focal hypodensity in the left fronto-temporal area
with clear mass effect as compressed left lateral ventricle.
Figure 2. a) First CT 3 hours after the onset of neurological symptoms shows unilateral hyperintense left middle cerebral artery. b) Blurred margins of
left lentiform nucleus. c) Control CT 4 days after the onset of neurological symptoms with clear focal hypodensity in the left fronto-temporal
area with massive mass effect in the form of compressed lateral ventricle and midline shift. d) Disappearance of visible left middle cerebral
artery which indicates lysis of the intra-arterial embolus; this confirms the vanishing nature of this sign.
effacement [1-3]. Major mass effect with midline Horowitz et al. [8] scanned 50 patients within the
shift does not appear before 12 hours after the first 3 hours. 28 patients (56%) showed evidence of
stroke onset. acute infarction on the first CT. These findings
included lentiform nucleus obscuring alone in 2
To study the prevalence of these finding, Toumora cases, hypodensity alone in 7, hypodensity with
et al. [1] evaluated CT scans within the first 6 hours mass effect in 15, and mass effect alone in 4
of ictus in 25 patients with involvement of the mid- patients.
dle cerebral artery MCA territory. 23 patients
(92%) demonstrated obscuring of the lentiform Another early highly specific, but less sensitive, sign
nucleus. Another study by Bozzao et al. [7] evalu- that has been extensively described is the unilateral
ated CT scans performed four hours from onset in hyperdense middle cerebral artery sign HMCAS,
36 patients with supratentorial stroke. 25 patients which is usually present in the first horizontal part
(69%) had abnormal CT, 14 patients obscuring of (M1). The specificity of this sign can reach 100%,
the lentiform nucleus alone, 5 patients findings but sensitivity is rather low, about 50% in the best
both in the lentiform nucleus and cerebral cortex, conditions. It is the reflection of a hyperintense
6 patients changes only in the cerebral cortex. embolus or thrombus lodged in this segment,
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Diagnostics and Medical Technology
defined as part of the MCA that is denser than its 4. Bell BA, Symon L, Branston NM: CBF and time threshold for the for-
contralateral counterpart or any other vessel of mation of ischemic cerebral edema, and effect of reperfusion in
similar size shown by an unenhanced CT where baboons. J Neurosurgery, 1985; 62: 31-41
the density could not be attributed to calcification 5. Schuir FJ, Hossman KA: Experimental brain infarction in cats.
and disappears on bone window, the incidence of Stroke, 1980; 11: 593-601
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50%. This wide variation has been attributed to 1983; 13: 2-10
slice thickness and whether strict or loose defini- 7. Bozzao L, Bastianello S, Fantozzi LM et al: Correlation of angio-
tion criteria have been followed [810]. graphic and sequential CT finding in patients with evolving cerebral
infarction. AJNR, 1989; 10: 1215-1222
The presence of hyperdense MCA has been con- 8. Horowitz SH, Zito JL, Donnarumma R et al: Computed tomographic
sidered as a poor prognostic sign associated with -angiographic finding within the first five hours of cerebral infarction.
severe neurological deficit and an indicator of Stroke, 1991; 22: 1245-1253
extensive infarct area. However, it is still uncertain 9. Pressman BD, Tourje EJ, Thompson JR: An early sign of ischemic
if HMCAS alone has any prognostic value [11,12]. infarction increased density in the middle cerebral artery. AJNR, 1987;
8: 645-648
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