Calcification of the basal ganglia: Difference between revisions
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(Created page with "π¬ Metabolic and Endocrine Causes 1. Hypoparathyroidism β most common systemic cause β’ β PTH β β calcium, β phosphate β’ Leads to symmetrical basal ganglia calcifications β’ May be idiopathic or post-surgical 2. Pseudohypoparathyroidism β’ PTH resistance; biochemical profile resembles hypoparathyroidism 3. Hyperparathyroidism β’ Less common, but can also lead to intracranial calcifications 4. Other metabolic disorders β’ Hypomagnesemia, hypop...") |
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π¬ Metabolic and Endocrine Causes | '''π¬ Metabolic and Endocrine Causes''' | ||
# Hypoparathyroidism β most common systemic cause | |||
#* β PTH β β calcium, β phosphate | |||
#* Leads to symmetrical basal ganglia calcifications | |||
#* May be idiopathic or post-surgical | |||
# Pseudohypoparathyroidism | |||
#* PTH resistance; biochemical profile resembles hypoparathyroidism | |||
# Hyperparathyroidism | |||
#* Less common, but can also lead to intracranial calcifications | |||
# Other metabolic disorders | |||
#* Hypomagnesemia, hypophosphatasia, mitochondrial cytopathies (like MELAS) | |||
'''𧬠Genetic and Degenerative Disorders''' | |||
# Fahrβs Disease (Idiopathic Basal Ganglia Calcification) | |||
#* Familial, autosomal dominant | |||
#* Progressive neurologic symptoms (parkinsonism, dementia, seizures) | |||
#* Normal calcium/phosphorus levels | |||
# Wilsonβs Disease | |||
#* Copper accumulation β may cause T2 hyperintensities or calcifications | |||
#* Neurologic and hepatic involvement | |||
# Mitochondrial disorders | |||
#* MELAS, Leigh syndrome | |||
#* Often show basal ganglia abnormalities and calcifications | |||
'''β£οΈ Toxic/Environmental Causes''' | |||
# Lead poisoning | |||
#* Chronic exposure may lead to calcifications and cognitive/behavioral changes | |||
# Carbon monoxide poisoning | |||
#* Hypoxic damage β calcifications of globus pallidus over time | |||
'''π¦ Infectious Causes''' | |||
* Congenital infections (especially TORCH): | |||
** Toxoplasmosis, Cytomegalovirus (CMV) β classically cause periventricular or basal ganglia calcifications in neonates | |||
'''π§ Others''' | |||
π§ͺ Workup Suggestion (in symptomatic or extensive cases) | * Radiation therapy | ||
* Chronic neuroinflammation | |||
'''π§ͺ Workup Suggestion (in symptomatic or extensive cases)''' | |||
* Serum calcium, phosphate, PTH, magnesium | |||
* Vitamin D levels | |||
* Brain CT (best to detect calcifications) | |||
* Consider genetic testing if familial or Fahrβs suspected | |||
* Toxicology screen if exposure suspected |
Latest revision as of 07:52, 4 June 2025
π¬ Metabolic and Endocrine Causes
- Hypoparathyroidism β most common systemic cause
- β PTH β β calcium, β phosphate
- Leads to symmetrical basal ganglia calcifications
- May be idiopathic or post-surgical
- Pseudohypoparathyroidism
- PTH resistance; biochemical profile resembles hypoparathyroidism
- Hyperparathyroidism
- Less common, but can also lead to intracranial calcifications
- Other metabolic disorders
- Hypomagnesemia, hypophosphatasia, mitochondrial cytopathies (like MELAS)
𧬠Genetic and Degenerative Disorders
- Fahrβs Disease (Idiopathic Basal Ganglia Calcification)
- Familial, autosomal dominant
- Progressive neurologic symptoms (parkinsonism, dementia, seizures)
- Normal calcium/phosphorus levels
- Wilsonβs Disease
- Copper accumulation β may cause T2 hyperintensities or calcifications
- Neurologic and hepatic involvement
- Mitochondrial disorders
- MELAS, Leigh syndrome
- Often show basal ganglia abnormalities and calcifications
β£οΈ Toxic/Environmental Causes
- Lead poisoning
- Chronic exposure may lead to calcifications and cognitive/behavioral changes
- Carbon monoxide poisoning
- Hypoxic damage β calcifications of globus pallidus over time
π¦ Infectious Causes
- Congenital infections (especially TORCH):
- Toxoplasmosis, Cytomegalovirus (CMV) β classically cause periventricular or basal ganglia calcifications in neonates
π§ Others
- Radiation therapy
- Chronic neuroinflammation
π§ͺ Workup Suggestion (in symptomatic or extensive cases)
- Serum calcium, phosphate, PTH, magnesium
- Vitamin D levels
- Brain CT (best to detect calcifications)
- Consider genetic testing if familial or Fahrβs suspected
- Toxicology screen if exposure suspected