Evaluation of neuroimaging findings in thalamic lesions: what can we think?

The diseases that affect the thalamus are heterogeneous in their etiologies, including infectious, inflammatory, vascular, toxic-metabolic, and neoplastic causes. It is often difficult to make the clinical differentiation between different entities. Within this context, computed tomography and magnetic resonance imaging have come to be of fundamental importance for defining the etiology and planning the treatment. In this pictorial essay, we will illustrate the main causes of diseases affecting the thalamus, discussing the possible differential diagnoses, as well as the most relevant imaging aspects.

Keywords:
Thalamus; Magnetic resonance imaging; Tomography, X-ray computed; Demyelinating diseases; Infections

Authorship

Bruno Niemeyer de Freitas Ribeiro Correspondence: Dr. Bruno Niemeyer de Freitas Ribeiro. Instituto Estadual do Cérebro Paulo Niemeyer - Departamento de Radiologia. Rua do Rezende, 156, Centro. Rio de Janeiro, RJ, Brazil, 20231-092. Email: bruno.niemeyer@hotmail.com.

Department of Radiology, Instituto Estadual do Cérebro Paulo Niemeyer, Rio de Janeiro, RJ, Brazil.Instituto Estadual do Cérebro Paulo NiemeyerBrazilRio de Janeiro, RJ, BrazilDepartment of Radiology, Instituto Estadual do Cérebro Paulo Niemeyer, Rio de Janeiro, RJ, Brazil.

Department of Radiology, Hospital Casa de Portugal / 3D Diagnóstico por Imagem, Rio de Janeiro, RJ, Brazil.Hospital Casa de Portugal / 3D Diagnóstico por ImagemBrazilRio de Janeiro, RJ, BrazilDepartment of Radiology, Hospital Casa de Portugal / 3D Diagnóstico por Imagem, Rio de Janeiro, RJ, Brazil.

https://orcid.org/0000-0002-1936-3026

Edson Marchiori

Universidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ, Brazil.Universidade Federal do Rio de JaneiroBrazilRio de Janeiro, RJ, BrazilUniversidade Federal do Rio de Janeiro (UFRJ), Rio de Janeiro, RJ, Brazil.

https://orcid.org/0000-0001-8797-7380

Correspondence: Dr. Bruno Niemeyer de Freitas Ribeiro. Instituto Estadual do Cérebro Paulo Niemeyer - Departamento de Radiologia. Rua do Rezende, 156, Centro. Rio de Janeiro, RJ, Brazil, 20231-092. Email: bruno.niemeyer@hotmail.com.

SCIMAGO INSTITUTIONS RANKINGS

Figures

Figures (11)

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Figure 1.
Creutzfeldt–Jakob disease in a patient with rapidly progressive cognitive decline. Axial FLAIR MRI sequence showing bilateral areas of hyperintensity in the thalamus (arrows), as well as in the caudate and lentiform nuclei (asterisks).

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Figure 2.
Neurotoxoplasmosis in a patient with acquired immunodeficiency syndrome who had a CD4 cell count of 126 cells/mm3. A: Axial FLAIR MRI sequence showing multiple hyperintense lesions in the nucleocapsular regions and in the left thalamus (arrow), with the eccentric target sign in the most medial lesion in the left thalamus (arrowhead). B: Contrast-enhanced axial T1-weighted MRI sequence showing nodular peripheral enhancement of the thalamic lesions (arrows).

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Figure 3.
Acute disseminated encephalomyelitis after viral infection. A: Axial FLAIR MRI sequence showing multiple hyperintense lesions throughout the white matter on both sides (arrowheads) and slightly affecting the left thalamus (arrow). B: Contrast-enhanced axial T1-weighted MRI sequence, acquired at a higher level, showing nodular enhancement of some lesions (arrowheads) and discontinuous annular enhancement (arrow) characteristic of demyelinating lesions.

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Figure 4.
Deep cerebral venous thrombosis in a female patient who used oral contraceptives. A: Axial FLAIR MRI sequence showing hyperintensity and a volume increase in the thalamus (arrows). B: Axial T2*-weighted MRI sequence showing hypointense foci within thalamic lesions (arrows), secondary to hemoglobin degradation products. C: Sagittal-enhanced axial T1-weighted MRI sequence showing a filling defect affecting the straight sinus (arrows). Source: Courtesy of Dr. Márcio Tadeu Vieira de Brito.

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Figure 5.
Bilateral thalamic infarcts in a patient with a sudden decrease in the level of consciousness. A: Axial CT slice showing areas of hypodensity in the thalamus (arrows). B: Axial FLAIR MRI sequence showing areas of hyperintensity in the thalamus (arrows).

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Figure 6.
Severe hypoxic-ischemic encephalopathy. Axial T2-weighted MRI sequence showing areas of hypodensity, together with volume reductions, in the thalamus (arrows) and the nucleocapsular region (asterisk). Note also the pronounced diffuse thinning of the white matter.

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Figure 7.
Wernicke’s encephalopathy in a malnourished alcoholic patient. A: Axial FLAIR MRI sequence showing symmetric areas of hyperintensity in the paraventricular regions of the thalamus (arrows). B: Axial FLAIR MRI sequence showing hyperintensity in the periaqueductal region (arrow).

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Figure 8.
Status epilepticus secondary to eclampsia. A: Coronal short-tau inversion recovery MRI sequence showing hyperintensity in the left thalamus (arrow). B: Axial DfMRI sequence showing hyperintensity in the pulvinar region of the left thalamus (arrow), as well as in the cortices of the ipsilateral temporal and occipital lobes (arrowhead).

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Figure 9.
Other toxic-metabolic and degenerative causes of thalamic lesions. A: Axial T2-weighted MRI sequence showing small hyperintense foci in the thalamus and nucleocapsular regions (arrows) in a six-year-old patient with neurofibromatosis type 1 (image courtesy of Dr. Márcio Tadeu Vieira de Brito). B: Axial CT slice showing calcifications in the thalamus and nucleocapsular regions (arrows) in a patient with Fahr’s disease who presented with progressive psychosis.

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Figure 10.
Histopathologically proven diffuse midline glioma with a histone H3-K27M mutation. A: Axial FLAIR MRI sequence showing an expansile hyperintense lesion in the right thalamus (arrow). B: Axial DfMRI sequence demonstrating hyperintense foci (arrows) within the lesion shown in A.

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Figure 11.
Metastases in a patient with clear cell renal cell carcinoma. Contrast- enhanced axial T1-weighted MRI sequence showing an expansile lesion, with contrast uptake, in the right thalamus, as well as other multiple lesions on both sides (arrowheads).

Figure 1. Creutzfeldt–Jakob disease in a patient with rapidly progressive cognitive decline. Axial FLAIR MRI sequence showing bilateral areas of hyperintensity in the thalamus (arrows), as well as in the caudate and lentiform nuclei (asterisks).

Figure 2. Neurotoxoplasmosis in a patient with acquired immunodeficiency syndrome who had a CD4 cell count of 126 cells/mm3. A: Axial FLAIR MRI sequence showing multiple hyperintense lesions in the nucleocapsular regions and in the left thalamus (arrow), with the eccentric target sign in the most medial lesion in the left thalamus (arrowhead). B: Contrast-enhanced axial T1-weighted MRI sequence showing nodular peripheral enhancement of the thalamic lesions (arrows).

Figure 3. Acute disseminated encephalomyelitis after viral infection. A: Axial FLAIR MRI sequence showing multiple hyperintense lesions throughout the white matter on both sides (arrowheads) and slightly affecting the left thalamus (arrow). B: Contrast-enhanced axial T1-weighted MRI sequence, acquired at a higher level, showing nodular enhancement of some lesions (arrowheads) and discontinuous annular enhancement (arrow) characteristic of demyelinating lesions.

Figure 4. Deep cerebral venous thrombosis in a female patient who used oral contraceptives. A: Axial FLAIR MRI sequence showing hyperintensity and a volume increase in the thalamus (arrows). B: Axial T2*-weighted MRI sequence showing hypointense foci within thalamic lesions (arrows), secondary to hemoglobin degradation products. C: Sagittal-enhanced axial T1-weighted MRI sequence showing a filling defect affecting the straight sinus (arrows). Source: Courtesy of Dr. Márcio Tadeu Vieira de Brito.

Figure 5. Bilateral thalamic infarcts in a patient with a sudden decrease in the level of consciousness. A: Axial CT slice showing areas of hypodensity in the thalamus (arrows). B: Axial FLAIR MRI sequence showing areas of hyperintensity in the thalamus (arrows).

Figure 6. Severe hypoxic-ischemic encephalopathy. Axial T2-weighted MRI sequence showing areas of hypodensity, together with volume reductions, in the thalamus (arrows) and the nucleocapsular region (asterisk). Note also the pronounced diffuse thinning of the white matter.

Figure 7. Wernicke’s encephalopathy in a malnourished alcoholic patient. A: Axial FLAIR MRI sequence showing symmetric areas of hyperintensity in the paraventricular regions of the thalamus (arrows). B: Axial FLAIR MRI sequence showing hyperintensity in the periaqueductal region (arrow).

Figure 8. Status epilepticus secondary to eclampsia. A: Coronal short-tau inversion recovery MRI sequence showing hyperintensity in the left thalamus (arrow). B: Axial DfMRI sequence showing hyperintensity in the pulvinar region of the left thalamus (arrow), as well as in the cortices of the ipsilateral temporal and occipital lobes (arrowhead).

Figure 9. Other toxic-metabolic and degenerative causes of thalamic lesions. A: Axial T2-weighted MRI sequence showing small hyperintense foci in the thalamus and nucleocapsular regions (arrows) in a six-year-old patient with neurofibromatosis type 1 (image courtesy of Dr. Márcio Tadeu Vieira de Brito). B: Axial CT slice showing calcifications in the thalamus and nucleocapsular regions (arrows) in a patient with Fahr’s disease who presented with progressive psychosis.

Figure 10. Histopathologically proven diffuse midline glioma with a histone H3-K27M mutation. A: Axial FLAIR MRI sequence showing an expansile hyperintense lesion in the right thalamus (arrow). B: Axial DfMRI sequence demonstrating hyperintense foci (arrows) within the lesion shown in A.

Figure 11. Metastases in a patient with clear cell renal cell carcinoma. Contrast- enhanced axial T1-weighted MRI sequence showing an expansile lesion, with contrast uptake, in the right thalamus, as well as other multiple lesions on both sides (arrowheads).

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