DOI: 10.1148/radiol.2341030252
(Radiology 2005;234:242-243.)
© RSNA, 2005
The Disappearing Basal Ganglia Sign1
Rocky C. Saenz, DO
1 From the Department of Radiology, Botsford General Hospital, 28050 Grand River Ave, Farmington Hills, MI 48336. Received February 23, 2003; revision requested May 16; final revision received September 24; accepted October 21. Address correspondence to the author, 21722 Malden St, Farmington Hills, MI 48336 (e-mail: dr.rocky@gmail.com).
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APPEARANCE
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The disappearing basal ganglia sign is a finding that can be seen at computed tomography (CT). It appears as a loss of the normal delineation of the basal ganglia, with the affected basal ganglia exhibiting abnormal morphologic features. This is best appreciated when a comparison is made between the affected basal ganglia and the contralateral side of the brain (Figs 1, 2).
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Figure 1a. Transverse CT scans obtained without intravenous contrast material demonstrate the disappearing basal ganglia sign. (a) Note the loss of the normal contour of the right basal ganglia. The left basal ganglia (arrow) are normal. The right insular cortex is obscured, and there is a loss of the gray matter-white matter junction. (b) Transverse CT scan from the same patient 36 hours later. The right middle cerebral artery (MCA) infarct (arrows) has now matured, creating a large area of hypoattenuation in the right basal ganglia, right temporal lobe, and posterior portion of the right frontal lobe. The left basal ganglia retain normal morphologic features and attenuation.
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Figure 1b. Transverse CT scans obtained without intravenous contrast material demonstrate the disappearing basal ganglia sign. (a) Note the loss of the normal contour of the right basal ganglia. The left basal ganglia (arrow) are normal. The right insular cortex is obscured, and there is a loss of the gray matter-white matter junction. (b) Transverse CT scan from the same patient 36 hours later. The right middle cerebral artery (MCA) infarct (arrows) has now matured, creating a large area of hypoattenuation in the right basal ganglia, right temporal lobe, and posterior portion of the right frontal lobe. The left basal ganglia retain normal morphologic features and attenuation.
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Figure 2a. Transverse CT scans obtained without intravenous contrast material demonstrate the disappearing basal ganglia sign. (a) Note the loss of the normal contour of the left basal ganglia. The right basal ganglia (arrow) are normal. The lentiform nucleus on the left has an area of hypoattenuation within it. Hypoattenuation is specifically located in the posterior portion of the putamen. Notice the left lentiform nucleus is much smaller than the right lentiform nucleus. The left insular cortex is obscured, and there is a loss of the gray matter-white matter junction. (b) Transverse CT scan from the same patient 24 hours later. The left MCA infarct (arrows) has now matured, creating a large area of hypoattenuation in the left basal ganglia, left temporal lobe, and posterior portion of the left frontal lobe.
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View larger version (137K):
[in this window]
[in a new window]
[Download PPT slide]
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Figure 2b. Transverse CT scans obtained without intravenous contrast material demonstrate the disappearing basal ganglia sign. (a) Note the loss of the normal contour of the left basal ganglia. The right basal ganglia (arrow) are normal. The lentiform nucleus on the left has an area of hypoattenuation within it. Hypoattenuation is specifically located in the posterior portion of the putamen. Notice the left lentiform nucleus is much smaller than the right lentiform nucleus. The left insular cortex is obscured, and there is a loss of the gray matter-white matter junction. (b) Transverse CT scan from the same patient 24 hours later. The left MCA infarct (arrows) has now matured, creating a large area of hypoattenuation in the left basal ganglia, left temporal lobe, and posterior portion of the left frontal lobe.
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EXPLANATION
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The disappearing basal ganglia sign is representative of cerebral infarction (1–3). The sign is usually caused by incomplete to complete occlusion of the MCA as a result of thromboembolic disease. Other differential diagnostic considerations include arterial dissection, trauma, vasculitis, and hemolytic uremic syndrome (4,5). If injury occurs bilaterally, diagnostic considerations include global hypoperfusion; respiratory arrest; near drowning; strangling; barbiturate overdose; methanol toxicity; cyanide poisoning; osmotic myelinolysis; hypoglycemia; Leigh disease; mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (also known as MELAS); and infectious causes (4,5).
Normally, the lentiform nucleus and caudate nucleus are slightly hyperattenuated when compared with the surrounding white matter. When present, a vascular insult will usually manifest at CT as areas of hypoattenuation, which occur when the normal cellular requirements are not met. Normal cell volume must be maintained with normal intra- and extracellular electrolyte concentration gradients. When there is an interruption of blood flow, cellular injury occurs. This, in turn, causes a loss of homeostasis and creates an influx of sodium, chloride, calcium, and water into the cells, thereby causing metabolic acidosis (6). This intracellular influx of fluid will lead to cytotoxic edema. The areas of hypoattenuation may also be interpreted as an indicator of severe focal ischemia (7).
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DISCUSSION
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The demonstration of a cerebral vascular accident at CT is important because early detection can aid in the decision to use thrombolytic therapy. Thrombolytic therapy has shown to be beneficial in improving patient outcome (8).
The majority of ischemic vascular accidents occur in the MCA territory (1). The most common causes of cerebral infarction in industrialized countries is thromboembolism (6,8). The causes of these emboli vary and may be secondary to atherosclerotic debris and arterial stenosis or of cardiac origin. The basal ganglia are susceptible to ischemic injury because the blood supply is derived from small arteries (6).
The basal ganglia are the masses of gray matter deep within the cerebral hemispheres. The basal ganglia include the caudate nucleus, amygdala, claustrum, internal capsule, external capsule, extreme capsule, and lentiform nucleus. The lentiform nucleus comprises the globus pallidus and putamen. The caudate nucleus, globus pallidus, and putamen are collectively referred to as the corpora striatum.
The basal ganglia derive their blood supply from the lenticulostriate arteries (5,6). A portion of the anterior limb of the internal capsule and the head of the caudate nucleus are supplied by the medial lenticulostriate arteries, which originate from the A1 segment of the anterior cerebral artery. The recurrent artery of Heubner is a major branch of the medial lenticulostriate arteries. The recurrent artery of Heubner may originate from the A1 or A2 segments of the anterior cerebral artery, but it most commonly originates (in 50% of population) from the A2 segment near the anterior communicating artery (5). The lateral lenticulostriate arteries supply the lentiform nucleus and parts of the caudate nucleus and internal capsule. There are approximately six to 20 lateral lenticulostriate arteries, which originate from the superior portion of the M1 segment of the MCA (9).
Early CT signs of MCA infarction include hyperattenuation of the MCA, an obscured lentiform nucleus, an obscured sylvian fissure, loss of the gray-white matter junction, and loss of the delineation of the basal ganglia (3,8,10). Findings from a study by Nakano et al (11) showed that early CT signs within the basal ganglia have a sensitivity of 77% and specificity of 100% for demonstrating cerebral vascular accident.
In conclusion, recognizing subtle changes within the basal ganglia, such as the disappearing basal ganglia sign, is important as an indicator of acute ischemic infarction.
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FOOTNOTES
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Author stated no financial relationship to disclose.
A trainee (resident or fellow) wishing to submit a manuscript for Signs in Imaging should first write to the Editor for approval of the sign to be prepared, to avoid duplicate preparation of the same sign.
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