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CNS manifestations related to parathyroid hormone (PTH) metabolic abnormalities
Hyperparathyroid (HPTH); hypoparathyroid (HP)
Bilateral symmetric calcifications in globi pallidi, putamen, caudate nuclei
Diffuse patchy “salt & pepper” lesions in skull in primary HPTH
Plaque-like dural calcification, “pipestem” calcifications of carotid arteries in secondary HPTH
Brown tumors: Focal expansile lytic lesions with nonsclerotic margins in primary HPTH and secondary HPTH
T2WI: Hypointensity involving basal ganglia, cerebral cortex, or dentate nucleus due to Ca++ deposition
Fahr disease
Physiologic calcification
Congenital HIV
Hypoxic-ischemic encephalopathy
Primary HPTH: Parathyroid adenoma (75-85%), parathyroid hyperplasia (10-20%), carcinoma (1-5%), ↑ PTH, ↑ Ca++
Secondary HPTH: Chronic renal failure, kidney fails to convert vitamin D to active form and excrete phosphate
HP: Parathyroids are absent or atrophied; genetic autoimmune syndrome or DiGeorge syndrome (total absence of PT glands at birth)
PHP: Insensitivity of end-organ to PTH, rather than decreased production of PTH
HPTH: ↑ Ca++ affects transsynaptic nerve conduction, fatigue, pain, nausea, osteoporosis
HP: Carpal-pedal spasm, tetany, seizure, and hyperreflexia
and sclerotic areas
involving the calvaria. This gives a classic salt and pepper appearance of the calvaria.
, sclerosis of calvaria
, and pipe-like calcification of the internal carotid arteries
.
. Focal calcifications are also seen in the subcortical white matter
.
due to calcifications. Calcium deposition in the basal ganglia is seen in both hyper- and hypoparathyroidism. Additional sites for calcium deposition include thalamus, subcortical white matter, dentate nuclei, and dura.
CNS manifestations related to parathyroid hormone (PTH) metabolic abnormalities
1° and 2° hyperparathyroidism (HPTH)
Hypoparathyroidism (HP)
Pseudohypoparathyroidism (PHP)
Pseudo-pseudohypoparathyroidism (PPHP)
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