A Radiological Approach to the Systemic and Neurologic Features of Hyperparathyroidism

Abstract

Parathyroid hormone (PTH) affects the nervous system directly and indirectly. The induced pathology may present typical imaging findings in neuroradiology. The hormone controls the physiological level of blood calcium. Increased serum PTH causes pathological features in the kidneys and especially in the skeleton where most calcium is situated.

Primary hyperparathyroidism is due to hyperplasia or to adenomatous or carcinomatous degeneration of glandular tissue. It causes relapsing nephrolithiasis and, more seldon, nephrocalcinosis. Bone shows increased osteoclastic activity with various aspects of diffuse demineralization. In severe cases pathological fractures and sub-periosteal, sub-chondral reabsorptions appear, especially at the tendon and capsuloligamentous insertions. In even more severe disease fibrous osseous cysts and brown tumours may be found in bone.

In the central nervous system, clinical symptoms, such as mental confusion, lethargy and exceptionally coma may appear. Radiologically, bone resorption can be observed in the skull as microlacunar confluent osteolysis (salt and pepper skull). Body fractures may develop in the spine.

Secondary hyperparathyroidism is due principally to renal failure. Both hypocalcaemia and hyperphosphoraemia cause the hormone secretion increase. In this case, other pathologic features are associated with the typical manifestations of primary hyperparathyroidism.

The uraemic kidney is inable to synthetize active vitamin D, leading to rickets in the young and osteomalacia in adults. Hyperphosphoraemia causes ectopic periarticular calcifications. Furthermore, the lack of degradation of an endogenous protein (beta 2 microglobulin) by the kidney and its poor elimination by dialytic treatment, cause chronic retention and consequent systemic amyloidosis which induces intraosseous cystic lesions and severe destructive arthropathy. All these aspects, together, are known as renal osteodystrophy.

The radiological features of secondary hyperparathyroidism are the same as those observed in the primary form. In addition, all the lesions of renal osteodystrophy may be associated, further worsening the disease.

In the secondary form, mild hypocalcaemia, if present, rarely leads to the neurological manifestations of the primary disease. Frequently carpal tunnel syndrome arises due to local amyloid infarction. Chronic aluminium retention may produce neurological aspects of dementia.

Finally, the decrease of PTH hormone blood levels, as in hypoparathyroidism and the consequent hypocalcaemia may determine neurologic symptoms such as paresthaesias, and in severe disease, tetanic contractions. Radiologically, typical micronodular calcifications can be observed in the brain basal ganglia.