Describing thalamic and basal ganglia abnormalities on brain computed tomography (CT)

Learn how to recognize abnormalities of the basal ganglia and thalami on CT, and their possible underlying causes.
Last update4th Jan 2021

Let’s talk about how to recognize abnormalities involving the basal ganglia and thalami on computed tomography (CT). Generally speaking, bilateral abnormalities involving the basal ganglia typically occur due to metabolic insults such as insufficient oxygen delivery or poisoning, while abnormalities of the thalami can be due to deep venous occlusion or infarcts.

Abnormalities in the basal ganglia on CT

When considering basal ganglia abnormalities on CT, the first step is to recognize what the normal basal ganglia look like. You should be able to see the lentiform nucleus (which consists of the globus pallidus and the putamen) on all normal CT scans because they all have a slightly higher attenuation than the surrounding white matter.

Figure 1. On normal computed tomography (CT) scans of the basal ganglia, you should be able to see the lentiform nucleus, which consists of the globus pallidus and the putamen, because they all have a slightly higher attenuation than the surrounding white matter.

Because of their high metabolic rate, the basal ganglia are particularly sensitive to metabolic injury from low blood flow, low levels of oxygen, and low glucose that can result in symmetric injuries of the basal ganglia.

Unilateral and bilateral basal ganglia abnormalities have different causes

While unilateral basal ganglia abnormalities are common with infarctions, infections, and brain tumors, bilateral basal ganglia abnormalities are usually the result of lack of oxygen seen with near-drownings, respiratory failure from a drug overdose, or low perfusion from cardiac arrest.

You should also consider poisoning as the cause of bilateral basal ganglia abnormalities, which can happen with carbon monoxide poisoning and toxic ingestions. For example, methanol ingestion has taken on new significance with reports of methanol-based hand sanitizer ingestion and skin absorption during the early days of the COVID-19 pandemic.

Figure 2. Causes of basal ganglia abnormalities on computed tomography (CT). Bilateral basal ganglia abnormalities are caused by low blood flow, low levels of oxygen, low glucose, and poisoning. Unilateral basal ganglia abnormalities are common with infarctions, infection, and brain tumors.

Case 1: Bilateral basal ganglia abnormalities due to methanol poisoning

Now that you know how the basal ganglia should look, you should be able to recognize the basal ganglia as symmetrically abnormal in our first patient case. On CT, notice how both sides of the basal ganglia are low in attenuation (Fig. 3). This patient ingested methanol in a suicide attempt that resulted in a bilateral basal ganglia injury.

The abnormality is more evident on magnetic resonance imaging (MRI), where mixed low and high signals due to both edema and hemorrhaging can be seen, which is typical of methanol poisoning.

Figure 3. A computed tomography (CT) scan from a patient who ingested methanol which shows basal ganglia that are symmetrically abnormal with low attenuation along with a magnetic resonance imaging (MRI) scan showing mixed low and high signal due to edema and hemorrhage that is typical with methanol poisoning.

Case 2: Bilateral basal ganglia abnormalities due to carbon monoxide poisoning

The second case we will examine also demonstrates a symmetrical basal ganglia abnormality. Here, in a 41-year-old with carbon monoxide poisoning, only the medial part of the lentiform nucleus is involved. Focal involvement of the globus pallidus has been reported with carbon monoxide poisoning. But, it is not specific for carbon monoxide poisoning since it can also be seen in other conditions such as drug overdose.

Figure 4. Computed tomography (CT) scans of a symmetrical basal ganglia abnormality in a 41-year-old with carbon monoxide poisoning where only the medial part of the lentiform nucleus is involved (Image courtesy of Dr S. Mohan. Associate Professor of Radiology, Hospital of the University of Pennsylvania).

Case 3: Bilateral basal ganglia abnormalities due to cardiac arrest

In clinical practice, basal ganglia abnormalities are often missed because the changes can be quite subtle on CT, and may be attributed to suboptimal CT scan quality. For example, a CT of a resuscitated 74-year-old man who was found unconscious after cardiac arrest shows the blurring of the border of the basal ganglia—if you are looking for it!

Figure 5. Bilateral basal ganglia abnormality on a computed tomography (CT) scan with a blurring of the border of the basal ganglia.

Case 4: Bilateral basal ganglia abnormalities after cardiac arrest in a child

Our fourth case involves a child who experienced cardiac arrest after major trauma. Her emergency room CT shows the blurring of the basal ganglia as well as at the gray-white matter interface on both cerebral hemispheres. One of the challenges of reading head CT is that you must recognize what is missing. When you look at the child’s CT scan alongside a CT from a patient with normal basal ganglia, the abnormality is much more evident.

Figure 6. Computed tomography (CT) scan from a child who experienced cardiac arrest after trauma showing blurring of the basal ganglia and at the gray-white matter interface on both cerebral hemispheres, beside a CT scan showing normal basal ganglia from a different patient.

The child’s CT scan also demonstrated a diffuse abnormality of the cortex. This is more evident on the coronal reconstruction of the CT scan where you can see that the cerebellum has a higher attenuation than the cortex of the hemispheres. This is called the white cerebellum sign and can help you identify a diffuse, hypoxic insult to the brain.

Figure 7. Computed tomography (CT) scans demonstrating a diffuse abnormality of the cortex which is more evident on the coronal reconstruction. The reconstruction shows the white cerebellum sign, where the cerebellum has a higher attenuation than the cortex of the hemispheres.

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Abnormalities in the thalami on CT

Posterior and immediately adjacent to the lateral border of the third ventricle is the thalami. These structures also have higher attenuation than white matter on CT, just like the basal ganglia. The lateral borders of the thalami are defined by the low attenuation posterior limbs of the internal capsule.

The thalamic blood supply arises almost entirely from the posterior circulation arteries, while the basal ganglia are supplied by perforators from the anterior circulation arteries arising from the carotids. The basal ganglia and thalami have a common venous drainage through the midline deep venous system.

Figure 8. The lateral borders of the thalami are defined by the low attenuation posterior limbs of the internal capsule.

Case 5: Bilateral basal ganglia and thalami abnormalities due to a deep venous occlusion

In our fifth case, the patient’s CT scan demonstrated low attenuation in the region of the basal ganglia and thalami. There is also evidence of hemorrhaging (Fig. 9). When you see this pattern of involvement of both the basal ganglia and thalami, you should consider the possibility of a deep venous occlusion since an arterial infarction is unlikely to involve both anterior and posterior perforating arteries.

Figure 9. Computed tomography (CT) scans from a patient with a cerebral deep venous occlusion demonstrating low attenuation in the region of the basal ganglia and thalami with evidence of a hemorrhage.

The sagittal reconstruction from a CT venography of the patient demonstrated a thrombus in the vein of Galen and the internal cerebral veins. Because of occlusion of the venous outflow, while there was continued arterial flow, the signal of the basal ganglia and thalami are altered due to venous hypertension.

One day later, a bilateral hemorrhage developed. This is another manifestation of venous hypertension. While the brain changes from venous occlusion in some patients are reversible, in this case, it resulted in a hemorrhagic infarction.

Figure 10. Sagittal reconstruction of a computed tomography (CT) venography from a patient with a cerebral deep venous occlusion demonstrating a thrombus in the vein of Galen and the internal cerebral veins beside a CT showing a bilateral hemorrhage which developed 1 day later.

Case 6: Bilateral thalami abnormalities due to dural fistula

When a 53-year-old was brought to the emergency room for persistent drowsiness, he received a contrast-enhanced CT scan. On the CT scan, the thalami do not have their normal high attenuation (Fig. 11).

The symmetrical thalamic abnormalities suggest the possibility of a deep venous occlusion. But, you can see that there is normal enhancement of both internal cerebral veins on the contrast-enhanced CT, which argues against thrombosis as the cause of the bilateral thalamic abnormalities.

Figure 11. Contrast-enhanced CT from a patient with persistent somnolence showing that the thalami do not have their normal high attenuation. But, both internal cerebral veins show normal enhancement, which argues against thrombosis as the cause.

The thalamic abnormalities were more apparent on the same patient’s magnetic resonance fluid-attenuated inversion recovery (FLAIR) scan. Even with the normal enhancement of the internal cerebral veins, a vascular cause was still suspected as the source of the patient’s symptoms. So, a digital subtraction angiography (DSA) was performed.

The DSA revealed the early appearance of the vein of Galen on a vertebral artery injection, which is a characteristic finding of a dural fistula. With an arteriovenous fistula (even though the deep venous system was open), the patient may have venous hypertension from the elevated, arterialized pressure in the venous system.

Figure 12. Magnetic resonance fluid-attenuated inversion recovery (FLAIR) scan from a patient with thalamic abnormalities beside a digital subtraction angiography (DSA) scan revealing the early appearance of the vein of Galen on a vertebral artery injection, which is a characteristic finding of a dural fistula.

Cases 7 and 8: Bilateral thalami abnormalities due to neoplasm

Our next cases involve two patients who also have bilateral thalamic abnormalities on MRI, but in their cases, it is due to neoplasm. Glial tumors can spread widely throughout the brain, so the tumor can spread from one thalamus to the other through a normal anatomic structure called the massa intermedia. This structure, also called the interthalamic adhesion, provides a bridge from one thalamus to the other.

Figure 13. Magnetic resonance imaging (MRI) scans from two different patients highlighting bilateral thalamic abnormalities due to neoplasm.

Case 9: Bilateral thalamic abnormalities due to an infarction

Bilateral thalami abnormalities can be the result of an infarction due to multiple emboli in the perforators that arise at the top of the basilar and posterior cerebral arteries.

Figure 14. Two magnetic resonance imaging (MRI) scans demonstrating bilateral thalami abnormalities due to infarction.

But, occlusion of the single artery of Percheron, a variation of the normal blood supply to the thalami, can also account for this appearance since it provides blood supply to both thalami in some patients.

Figure 15. The artery of Percheron.

Finally, Wernicke’s encephalopathy and osmotic demyelination can involve both thalami. But, the findings in such cases are almost always inapparent on CT.

A careful review of the history will be of considerable help in patients with bilateral disease involving the basal ganglia or thalami. When you see abnormalities of the basal ganglia, consider metabolic insults such as an insufficient supply of oxygen or poisoning. As well, abnormalities of the thalami on CT are usually due to infarctions or deep venous occlusions.

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Recommended reading

  • Kim, DS, Na, DG, Kim, KH, et al. 2009. Distinguishing tumefactive demyelinating lesions from glioma or central nervous system lymphoma: added value of unenhanced CT compared with conventional contrast-enhanced MR imaging. Radiology. 251: 467–475. PMID: 19261924

About the author

Alexander Mamourian, MD
Professor Emeritus of Radiology at the University of Pennsylvania and Professor of Radiology, Neurosurgery, and Neurology at Penn State, Hershey Medical Center, USA.
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