Files

T

Ross 1e36a4957c .

2025-10-20 08:40:33 +01:00

29 KiB

Raw Blame History

title, docid, authors, breadcrumbs, category, cmeTopicId, documentVersionId, imageCount, lastUpdated, pageDescription, pageKeywords, pageTitle, enhancedTitle, type, references, breadcrumbs

title

docid

authors

breadcrumbs

ESSENTIAL INFORMATION

Key Differential Diagnosis Issues
- Basal ganglia (BG) Ca⁺⁺ is end result of multiple toxic, metabolic, inflammatory, & infectious insults
- Location of Ca⁺⁺ helpful to determine underlying cause [globus pallidus (GP) vs. putamen vs. caudate]
- Patient age may impact differential diagnosis
Helpful Clues for Common Diagnoses
- Aging B****rain, Normal - Commonly affects GP more than putamen - Seen in aging brain as normal variant - Typically in patients older than 30 years - If occurs with other Ca⁺⁺, consider pathologic condition
- Neurocysticercosis - May occur anywhere in brain - Convexity subarachnoid spaces most common - Imaging varies with pathologic stage - Ca⁺⁺ in nodular calcified (healed) stage
Helpful Clues for Less Common Diagnoses
- Fahr Disease - Bilateral symmetric BG Ca⁺⁺, often with Ca⁺⁺ in other locations - GP is most common site of Ca⁺⁺ (lateral > medial) - Other locations: Putamen, caudate, thalami, dentate nuclei of cerebellum, cerebral white matter (WM), internal capsule - Associated abnormalities: Parkinsonism in autosomal dominant Fahr disease (FD)
- Hypoxic-Ischemic Injury - Term: Profound acute injury results in decreased BG & thalamic density ± hemorrhage acutely - Lateral thalami & posterior putamen typical - May show Ca⁺⁺ in chronic phase - Adults: Putamen > GP typically - May have history of anoxic event - MR > CT for acute changes - May show Ca⁺⁺ in chronic phase
- Mitochondrial Disorders - Mitochondrial myopathy, encephalopathy, lactic acidosis, & stroke-like episodes (MELAS): BG Ca⁺⁺ in child or young adult with cortical lesions (parietooccipital > temporoparietal) - Myoclonic epilepsy with ragged red fibers (MERRF): BG Ca⁺⁺ with watershed ischemia
- Congenital Infections - HIV, congenital - Symmetric BG Ca⁺⁺ & cerebral atrophy - GP & putamen > caudate - Subcortical WM Ca⁺⁺ common - Ca⁺⁺ occurs in fairly symmetric fashion, result of calcific vasculopathy of medium & small arteries - CMV, congenital - Periventricular Ca⁺⁺, microcephaly, & cortical dysplasia - Periventricular > > BG Ca⁺⁺
- Endocrinologic Disorders - Imaging of hyperparathyroidism, hypoparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism, hypothyroidism in nearly indistinguishable - Bilateral BG: GP & putamen, dentate nuclei, thalami, subcortical areas - Ca⁺⁺ in primary hypoparathyroidism is more diffuse than in other etiologies of Ca⁺⁺
- Toxoplasmosis, Acquired - Typically multifocal, but BG common site (up to 75%) - Enhancing lesion most common acutely - Post therapy, Ca⁺⁺ is common
- Leigh Syndrome - Bilateral, symmetric ↑ T2/FLAIR putamina & periaqueductal gray matter - Putamen > caudate > GP, Ca⁺⁺ when chronic
- Tuberculosis - Typically causes tuberculous meningitis &/or localized CNS infection, tuberculoma - ~ 20% of tuberculomas calcify
- Radiation**&**Chemotherapy - Mineralizing microangiopathy causes BG & subcortical WM Ca⁺⁺, atrophy - Mineralizing microangiopathy common with chemotherapy & XRT - Typically occurs 2 or more years after XRT
- Cavernous Malformation (Mimic) - Hyperdense mass (Ca⁺⁺ & blood products) may occur in any location
- Vascular Calcification (Mimic) - May relate to physiologic vascular calcification, atherosclerosis, aneurysm, or vascular mass
- Tuberous Sclerosis Complex (Mimic) - Subependymal nodules are typically calcified; occur along caudothalamic groove, periventricular
Helpful Clues for Rare Diagnoses
- Developmental Venous Anomaly - Congenital cerebral vascular malformation with mature venous elements - "Medusa head" with many small veins joining into collector vein - Seen on contrast CT/MR, CTA/CTV, MRV, DSA, SWI - Unilateral BG/thalami Ca⁺⁺ rare - May be related to venous congestion/ischemia
- Pantothenate Kinase-Associated Neurodegeneration - Rare neurodegenerative disorder with brain iron accumulation - T2 MR characteristic: High signal within bilateral GP with surrounding low signal, eye of the tiger appearance - CT may show mineralization in GP - Formerly known as Hallervorden-Spatz
- Carbon Monoxide Poisoning - Typically hypodense, symmetric GP on CT, T2 hyperintense - GP Ca⁺⁺ occurs as end result
- Parasites, Miscellaneous - Amebic encephalitis: Supratentorial, frontal lobes, & BG - Typically enhancing lesions acutely, may calcify in chronic phase - Malaria: Predilection for BG, cortex - Hemorrhage, infarcts, & cerebral edema - May show Ca⁺⁺ in chronic phase - Paragonimiasis: Acutely often hemorrhage or infarct, followed by Ca⁺⁺ granulomas
Alternative Differential Approaches
- BG Ca⁺⁺ in child - Mitochondrial encephalopathies: MELAS, MERRF, Leigh syndrome - Congenital infections: HIV, CMV - HIE, term - Associated with Down syndrome - Aicardi-Goutières syndrome (pseudo-TORCH) - Cockayne syndrome - Long-term complications of radiation therapy for childhood brain tumors & intrathecal chemotherapy

References

Selected References

Images

Selected Images

Aging Brain, Normal Axial NECT shows typical basal ganglia (BG) Ca⁺⁺ in this 75-year-old man who presented after minor trauma. Note the location within the globus pallidus (GP) , typical for normal aging brain. Physiologic Ca⁺⁺ is typically seen in adults over 30 years.

Neurocysticercosis Axial CT shows multiple calcified nodules in the deep gray nuclei & along the cortex related to the nodular, calcified (healed) stage of neurocysticercosis. This intracranial parasitic infection is caused by the pork tapeworm Taenia solium.

Fahr Disease Axial NECT shows the typical CT appearance of Fahr disease (FD) with extensive calcifications present in the BG, cerebral white matter (WM), & at the subcortical gray matter-WM junctions.

Hypoxic-Ischemic Injury Axial NECT shows calcification of thalami & BG from status marmoratus. There is atrophy & a collapsed calvarium following remote mixed hypoxic-ischemic injury (HII) in this infant. Profound acute HII typically affects the BG.

Mitochondrial Disorders Axial NECT in a teenager shows bilateral GP Ca⁺⁺, a rare finding in patients < 30 years.

Mitochondrial Disorders FLAIR MR (same patient) shows left frontal & parietal hyperintensity related to recent middle cerebral artery & anterior cerebral artery infarcts. Muscle biopsy showed myoclonic epilepsy with ragged-red fibers. This rare mitochondrial disorder often presents with myoclonus & seizures. Imaging mimics other mitochondrial disorders, incl. mitochondrial myopathy, encephalopathy, lactic acidosis, & stroke-like episodes (MELAS).

Mitochondrial Disorders Axial NECT shows Ca⁺⁺ of the GP bilaterally in this child with MELAS. Note the low density in the medial occipital lobes related to infarcts. BG Ca⁺⁺ is abnormal in children & young adults.

HIV, Congenital Axial NECT in a patient with congenital HIV shows bilateral symmetrical BG Ca⁺⁺ predominantly in the GP . This Ca⁺⁺ is seen typically months after birth. With HIV, involvement of the lentiform nuclei Ca⁺⁺ is greater than the caudate heads.

CMV, Congenital Axial NECT shows periventricular & BG Ca⁺⁺ as well as open Sylvian fissures & ventriculomegaly. Periventricular Ca⁺⁺, ventriculomegaly, & microcephaly strongly suggest congenital CMV infection.

Endocrinologic Disorders Axial NECT in a patient with with hypothyroidism shows diffuse hyperdense Ca⁺⁺ within the BG, thalami, & subcortical WM. Ca⁺⁺ related to systemic disease is typically symmetric.

Endocrinologic Disorders Axial NECT in a patient with pseudohypoparathyroidism shows dense Ca⁺⁺ within the BG & subcortical WM in a pseudohypoparathyroidism patient. There is significant imaging overlap between systemic diseases with abnormal calcium deposition.

Toxoplasmosis, Acquired Axial T1 C+ MR shows an enhancing right BG mass in an AIDS patient. Post therapy, enhancing lesions typically calcify. The BG is the most common location for toxoplasmosis followed by the thalamus, then the cerebral hemispheres.

Leigh Syndrome Axial T2WI MR shows symmetric T2 hyperintensity in the BG bilaterally in this child with neurodegeneration. Ca⁺⁺ of the BG is seen in chronic cases.

Radiation & Chemotherapy Axial NECT shows mineralizing microangiopathy related to radiation therapy & chemotherapy for a remote childhood neoplasm. Note the symmetric Ca⁺⁺ in the BG & subcortical WM. This typically occurs ~ 2 years after therapy with XRT & chemotherapy.

Tuberous Sclerosis Complex (Mimic) Axial T2 MR shows calcified subependymal nodules in the foramen of Monro region in this child with seizures, mimicking BG Ca⁺⁺. These nodules occur in 98% of patients with tuberous sclerosis.

Developmental Venous Anomaly Axial NECT shows dense Ca⁺⁺ in right BG & thalamus. CE images (not shown) revealed an underlying developmental venous anomaly. These are congenital cerebral vascular malformations with mature venous elements, which may rarely have Ca⁺⁺ possibly related to underlying venous congestion & ischemia.

Additional Images

Fahr Disease Axial NECT shows a variant CT appearance of FD with extensive Ca⁺⁺ present in the BG, cerebral WM, & at the subcortical gray matter-WM junctions.

Pantothenate Kinase-Associated Neurodegeneration Axial NECT shows globus pallidus mineralization bilaterally in a patient with pantothenate kinase-associated neurodegeneration. CT is typically normal. T2 MR shows classic the eye of the tiger appearance with globus pallidus hypointensity related to iron accumulation with medial T2 hyperintensity.

CMV, Congenital Axial NECT shows marked atrophy & minimal BG Ca⁺⁺ in this child with congenital CMV. The Ca⁺⁺ seen in CMV is typically asymmetric & associated with migrational abnormalities & microcephaly.

Radiation & Chemotherapy Axial NECT shows mineralizing microangiopathy related to radiation therapy & chemotherapy for a posterior fossa medulloblastoma. Note the symmetric Ca⁺⁺ in the BG & subcortical WM.

CMV, Congenital Axial NECT shows periventricular & BG Ca⁺⁺. Periventricular calcifications, ventriculomegaly, & microcephaly strongly suggest congenital CMV infection.

Toxoplasmosis, Acquired Axial CECT shows an enhancing BG mass in an AIDS patient. Post therapy, enhancing lesions typically calcify. BG is the most common location followed by thalamus, then hemispheres.

Vascular Calcification (Mimic) Axial NECT shows intracranial atherosclerotic disease with extensive Ca⁺⁺ in internal carotid & middle cerebral arteries , which mimics BG Ca⁺⁺. Posterior fossa aneurysm is partially visible.

Tuberous Sclerosis Complex (Mimic) Axial NECT shows calcified subependymal nodules in the foramen of Monro & periventricular regions, which mimic BG Ca⁺⁺. These typically accompany cortical tubers , better seen on MR.

Parasites, Miscellaneous Axial CECT shows a case of paragonimiasis with a hyperdense left BG nodule . This parasite often presents with conglomerated granulomas, which may hemorrhage. Multiple Ca⁺⁺ are common.

Neurocysticercosis Axial CECT shows a calcified left putamen nodule that represents the nodular, calcified (healed) stage of neurocysticercosis. Note the right external capsule cyst with a central "dot" representing a scolex.

Pseudohypoparathyroidism Axial NECT shows diffuse calcifications within the BG & subcortical WM in a pseudohypoparathyroidism patient. There is significant imaging overlap between systemic diseases with abnormal calcium deposition.

HIV, Congenital Axial NECT shows symmetric BG calcification with scattered foci of subcortical calcification. Note the typical HIV involvement of the lentiform nuclei is greater than the caudate heads.

29 KiB Raw Blame History

ESSENTIAL INFORMATION

Key Differential Diagnosis Issues

Helpful Clues for Common Diagnoses

Helpful Clues for Less Common Diagnoses

Helpful Clues for Rare Diagnoses

Alternative Differential Approaches