Question:

Regarding nonketotic hyperglycemia and the etiology of hyperattenuation seen on computed tomography and hyperintense T1 signal on magnetic resonance in the basal ganglia, which one of the following answer choices if false?
1. Hyperattenuation on computed tomography, whether in the caudate, putamen, or globus pallidus, respects neuroanatomic boundaries making hemorrhage a less likely etiology.
2. Lack of consistent hypointensity/blooming artifact on susceptibility-weighted imaging makes hemorrhage a less likely etiology.
3. Lack of the expected methemoglobin T2-weighted hyperintense evolution of blood products on follow-up imaging makes hemorrhage a less likely etiology.
4. Leading hypothesis states that T1 hyperintensity on magnetic resonance imaging is most likely due to "unwrapping of the myelin sheath" and swollen gemistocytes.
5. Edema associated with the basal ganglia abnormality on both magnetic resonance and computed tomography suggests hemorrhage is the most likely etiology.





Answer:

The correct answer for the question "Regarding nonketotic hyperglycemia and the etiology of hyperattenuation seen on computed tomography and hyperintense T1 signal on magnetic resonance in the basal ganglia, which one of the following answer choices if false?" is:

5. Edema associated with the basal ganglia abnormality on both magnetic resonance and computed tomography suggests hemorrhage is the most likely etiology.



Explanation
1. Hyperattenuation on computed tomography respects the neuroanatomic boundaries of the basal ganglia which is not consistent with the expected findings for hemorrhage. [However, blood products are felt to be a less likely etiology given the manner in which the T1 hyperintensity respects neuroanatomic boundaries, lack of consistent positive susceptibility-weighted findings and lack of expected methemoglobin T2-weighted hyperintense evolution.]

2. Hemorrhage is expected to bloom on susceptibility-weighted imaging if blood products account for the basal ganglia findings. [See explanation for answer choice number one.]

3. Follow-up imaging does not demonstrate the expected methemoglobin T2-weighted hyperintense evolution of blood products. [See explanation for answer choice number one.]

4. Most widely offered hypothesis for etiology of T1 hyperintensity involves swollen gemistocytes and pathology of the myelin sheath. [The most widely promoted hypothesis ascribes the T1 hyperintensity to the protein hydration layer in the cytoplasm of swollen gemistocytes (reactive astrocytes).]

5. No edema, on either computed tomography or magnetic resonance imaging, is associated with the basal ganglia lesions. [As with prior cases of nonketotic hyperglycemia, the imaging findings in the basal ganglia conformed to the neuroanatomic boundaries of the caudate nuclei and left lentiform nucleus without associated mass effect or edema.]



From the manuscript:
Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)
Radiology Case. 2013 Aug; 7(8):1-9


This article belongs to the Neuro section.




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From the manuscript

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Free full text article: Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Abstract
While there are broad differential diagnoses for either the clinical finding of hemichorea-hemiballism or the imaging finding of lateralizing/asymmetric basal ganglia lesions (hyperdense on computed tomography, hyperintense on T1 magnetic resonance imaging), the presence of both findings is highly suggestive of nonketotic hyperglycemia. We present an unusual case of a patient with vague stroke-like complaints and imaging findings notable for lateralizing basal ganglia lesions. Laboratory analysis revealed nonketotic hyperglycemia and neurologic exam failed to elicit any findings of movement disorder. As far as we know, this is the first published case of a patient with typical neuroimaging manifestations of nonketotic hyperglycemia without associated hemichorea-hemiballism (a disorder of abnormal movements comprised of more proximal, higher amplitude movements-ballismus and lower amplitude, more distal movements- chorea). This finding suggests that radiologists should be alert to the possibility of nonketotic hyperglycemia in patients with asymmetric/lateralizing basal ganglia lesions even in the absence of a movement disorder.






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